hyperthyroidism Flashcards

1
Q

what are the two subclasses in hyperthyroidism?

A

Graves’ diesease

Nodular Goitre/ Plummer’s disease (this is a benign tumour that produces thyroxine)

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2
Q

What is Graves disease?

A

Autoimmune condition.
Antibodies bind to and stimulate the TSH receptor in the thyroid, so more TSH is produced and therefore more T4/T3 produced

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3
Q

What are some of the signs for graves disease?

A
Cause goitre (smooth) and hyperthyroidism
Tremor 
Palpitation 
Diarrhea 
Muscular weakness 
Localised myxedma
Oligomenorrhea 
Rapid pulse 
Loss of weight 
Rapid pulse 
Shortness of breath 
Facial flushing 
Excessive sweating 
exophthalmos
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4
Q

what is exophthalmos?
Why is it caused in graves disease?
what does exopthalmos also lead to?

A

Exophthalmos= red, irritated eyes which pop out.
Other antibodies bind to muscles behind the eye causing the eye muscles to contract, pushing the whole eye forward and it causes exophthalmos
Chemosis= sincethe eyelids don’t fully shut, the eyes dry out leading to dry eyes

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5
Q

what is pretibial myxoedema?

A

The swelling (non-pitting) that occurs on the shins of patients with Graves’ disease: growth of soft tissue.

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6
Q

what is plummer’s disease?

And how is it different from Graves disease/

A
Toxic nodular goitre
NOT autoimmune
Benign adenoma that is overactive at making thyroxine.
NO pretibial myxoedema
NO exophthalmos
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7
Q

how does the enlargement of the thyroid gland differ in plummers and in graves?

A

in graves there is a smooth overall enlargement of the thyroid gland since there are receptors all around the gland.
In plummers, one side will shrink and the side with the tumour will grow. Shows up as a hot nodule.

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8
Q

what are the effects of thyroxine on the sympathetic nervous system, and what symptoms does this correlate to?

A

Sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline.
Thus there is apparent sympathetic activation
Tachycardia, palpitations, tremor in hands, lid lag (feature of too much adrenaline)

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9
Q

what are the common signs for hyperthyroidism?

A
Weight loss despite increased appetite
Breathlessness, 
palpitations, tachycardia
Sweating
Heat intolerance
Diarrhoea
Lid lag and other sympathetic features
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10
Q

what is a thyroid storm?

A

Thyroid storm is a life-threatening health condition that is associated with untreated or undertreated hyperthyroidism. During thyroid storm, an individual’s heart rate, blood pressure, and body temperature can soar to dangerously high levels.

Medical emergency : 50% mortality untreated
Blood results confirm hyperthyroidism

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11
Q

what are signs of a thyroid storm?

A
Hyperpyrexia (high fever) > 41oC
accelerated tachycardia / arrhythmia
cardiac failure
delirium / frank psychosis
hepatocellular dysfunction; jaundice
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12
Q

what are the treatment options for hyperthyroidism?

A

Surgery (thyroidectomy)
Radioiodine
Drugs

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13
Q

what is viral thyroiditis?

A

thyroiditis is a painful swelling of the thyroid gland thought to be triggered by a viral infection, such as mumps or the flu. the virus binds to the thyroid gland and irritates it and cuases pain and tenderness. This leads to the thyroid gland secreting all its thyroxine stores ino the circulating leading to symptoms similar to that of hyperthyroidism
Thyroid stops making thyroxine and makes viruses instead
Thus no iodine uptake (ZERO)

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14
Q

signs of viral thyroiditis

A
thyroid gland tender, palpable 
tender lymph nodes 
malaise 
pain radiating to ear 
thyroid gland enlarged and painful to touch
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15
Q

why do patients with viral thyroiditis become hypothyroid after a few weeks?

A

Radioiodine uptake zero
Stored thyroxine released
Thus toxic with zero uptake

Four weeks later, stored thyroxine exhausted, so hypothyroid.

After a further month, resolution occurs (like in all viral diseases).

Patient then becomes euthyroid again.

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16
Q

what are the classes of drugs used in the treatment of hyperthyroidism

A
  1. The thionamides (thiourylenes; anti-thyroid drugs)
    • propylthiouracil (PTU)
    • carbimazole (CBZ)
  2. Potassium Iodide
  3. Radioiodine
  4. β-blockers
17
Q

which of the drugs target hyperthyroidism and which help with symptoms?

A

Essentially, the first 3 drugs are aimed at blocking thyroxine synthesis and therefore target hyperthyroidism per se. Beta blockers help with symptoms

18
Q

when can thionamides be used?

A
  • daily treatment of hyperthyroid conditions, such as in graves and toxic thyroid nodule.
  • treatment prior to surgery
  • reduction of symptoms whilst waiting for radioactive iodine to act
19
Q

what is the mechanism of action of thionamides?

A
  1. inhibition of thyroid peroxidase and hence T3/T4 synthesis and secretion
  2. may suppress antibody production in Graves’ disease
  3. reduces conversion of T4 to T3 in peripheral tissues (PTU)
20
Q

why might you give propranolol alongside thionamides?

A

because the thionamides take a couple of weeks to show their effect, but propranolol rapidly reduces tremors and tachycardia

21
Q

what can be the unwanted actions of thionamides?

A

Agranulocytosis (usually reduction in neutrophils) - rare and reversible on withdrawal of drug. Ask the patient to come in for a blood test if they get a fever or a cold.
rashes (relatively common)

22
Q

what are the pharmacokinetics of thionamides?

A

orally active

ii) carbimazole is a pro-drug which first has to be converted to methimazole
iii) cross placenta, secreted in breastmilk (PTU less than CBZ)

23
Q

what’s the follow up for anti-thyroid drugs/thionamides?

A

Usually aim to stop anti-thyroid drug treatment after 18 months

Review patient periodically including thyroid function tests for remission/relapse

24
Q

what is the role of beta blockers in thyrotoxicosis (another term for hyperthyroidism)?

A

Several weeks for ATDs to have clinical effects such as reduced tremor, slower heart rate, less anxiety
whereas NON-selective (ie b1 & b2) b blocker
eg propranolol
achieves these effects in the interim (less so with selective b1 blockers eg atenolol)

25
Q

when can iodide (such as potassium iodide) be used?

A

preparation of hyperthyroid patients for surgery

severe thyrotoxic crisis (thyroid storm)

26
Q

what is the mechanism of KI?

A
  1. inhibits iodination of thyroglobulin

2. inhibits hydrogen peroxide generation and thyoperoxidase

27
Q

what does KI do chemically?

A

1.Inhibition of thyroid hormone synthesis & secretion
WOLFF–CHAIKOFF effect - presumed autoregulatory effect
2. hyperthyroid symptoms reduce within 1-2 days
3. vascularity and size of gland reduce within 10-14 days

28
Q

what is Wolff-chaikoff effect?

A

is a presumed reduction in thyroid hormone levels caused by ingestion of a large amount of iodine

29
Q

what are the unwanted effect of iodide?

A

Allergic reaction eg. rashes, fever, angio-oedema

30
Q

pharmacokinetics for iodide?

A

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

31
Q

what does radioiodine do?

mechanism

A

Treats hyperthyroidism (Graves’, toxic nodular disease), thyroid cancers

accumulates in colloid, emits beta particles destroying follicular cells

32
Q

what are the pharmokinetics for radioiodine?

A

Discontinue anti-thyroid drugs 7-10 days prior to radioiodine treatment

Administer as a single oral dose

Radioactive half life of 8 days

Radioactivity negligible after 2 months

33
Q

what do you need to be careful about when using radioiodine?

A

Avoid close contact with small children for several weeks after receiving radioiodine.
Contra-indicated in pregnancy and breast feeding

34
Q

what are the risks of thyroidectomy

A

damage to the parathyroid glands and recurrent laryngeal nerve (hoarse voice)