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eLCRS - 엔도 > Endo 5: Thyroid Disorders - Hyperthyroidism > Flashcards

Endo 5: Thyroid Disorders - Hyperthyroidism Flashcards

1
Q

What is a key characteristic of Grave’s Disease, and how does it occur?

A

Key characteristic= autoimmune disease

onset:
- antibodies bind to TSH receptor
- stimulates receptor in the thyroid

–> causes goitre + hyperthyroidism

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2
Q

What are other symptoms of Graves disease?

A
  • antibodies binding to muscles behind eye –> exophthalmos

- pretibial myxoedema

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3
Q

What is pretibial myxoedema ?

A

Pretibial Myxoedema:

- swelling (growth of soft tissue) that occurs on shin

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4
Q

What are key characteristics of Plummer’s Disease?

A

Plummer’s disease:

  • toxic nodular goitre
  • NOT autoimmune
  • benign adenoma –> overactive at making thyroxine
  • NO pretibial myxoedema
  • NO exophthalmos
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5
Q

Explain the effects of thyroxine on the SNS.

A
  • Thyroxine sensitises B-adrenoreceptors to ambient adrenaline/ noradrenaline levels
  • so there is apparent Sympathetic activation (but there isn’t - its just more sensitive??? )
  • results in tachycardia, palpitations, hand tremor, lid lag
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6
Q

List main symptoms of hyperthyroidism

A

(EVERYTHING SPEEDS UP)

  • weight loss, increased appetite
  • breathlessness
  • palpitations, tachycardia
  • sweating
  • heat intolerance
  • diarrhea
  • lid lag
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7
Q

What are characteristics of a thyroid storm?

A
  • hyprepyrexia >41deg C
  • accelerated tachycardia / arrhythmia
  • cardiac failure
  • delirium / frank psychosis
  • hepatocellular dysfunction; jaundice
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8
Q

What are treatment options for thyroid storm?

A
  • thyroidectomy
  • radioiodine
  • drugs
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9
Q

What are signs + symptoms of Viral Thyroiditis?

A
  • painful dysphagia
  • hyperthyroidism
  • pyrexia
  • raised ESR
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10
Q

What is the mechanism behind viral thyroiditis?

A
  • virus attacks thyroid gland
  • causes pain + tenderness
  • thyroid stops making thyroxine
  • makes virus instead
  • so no (ZERO) iodine uptake
  • stored thyroxine is released
  • so toxic with ZERO uptake

note: by 4 wks later, stored thyroxine = exhausted
- -> hypothyroid

by 1 month –> resolution occurs

patient becomes euthyroid again

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11
Q

What are the 4 classes of drugs used in the treatment of hyperthyroidism?

A
  1. thionamides
    - propylithiouracil
    - carbimazole
  2. potassium iodide
  3. radioiodine
  4. B-blockers

Note:
(1+2+3 = reduces thyroid hormone production)
(4 = relieves symptoms of thyrotoxicosis)

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12
Q

How are thionamides used?

What are they used for?

A
  • given as daily treatment of hyperthyroid conditions
    (e. g graves, toxic thyroid nodule etc.)
  • treatment prior to surgery
  • reduction of symptoms while waiting for radioactive iodine to act
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13
Q

Briefly describe the process of thyroid hormone synthesis .

A
  • iodine = taken up into follicular cells
  • through action of thyroperoxidase + H2O2 –> you get iodination of tyrosine residues (in thyroglobulin)
  • then coupling of mono/diiodotyrosine –> T3 + T4
  • taken up + released by cells into circulation
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14
Q

Describe the mechanism of action of Thionamides

A
  • Thionamides INHIBIT thyroperoxidase
  • so they inhibit iodination of thyroglobulin + coupling of iodotyrosines
  • net result = reduction in synthesis + secretion of thyroid hormones
  • also suppresses antibody production in Graves disease
  • reduced deidination of T4 –> T3 (in peripheral tissue)
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15
Q

How long does it take for clinical effects of thionamides to take place?

A
  • biochemical effect occurs in hours
    BUT
  • it takes WEEKS before clinical effects can be seen.

BECAUSE
- there is a lot of stored thyroid hormone in lumen of thyroid follicles
(doesn’t affect stored hormone)

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16
Q

Why would you want to manage symptoms in the shortterm with non selective beta blockers?

A
  • because there is a delayed clinical effect of thionamides (due to stored hormone)
  • takes several weeks for anti thyroid drugs to have clinical effects
17
Q

What are some unwanted actions of Thionamides?

A
  1. agranulocytosis –> reduction in neutrophils
    - reversible on withdrawal of drug
  2. rashes
18
Q

Describe 2 features of pharmacokinetics of thioamides

A
  1. orally active
  2. carbiamazole = pro drug which first has to be converted to methimazole
  3. crosses placenta –> and is secreted in breastmilk
  4. metabolized in liver + secreted in urine
19
Q

How would you follow up with the anti-thyroid drug treatment?

A
  • aim = stop treatment after 18 months

- review patient periodically
thyroid function tests for remission/relapse

20
Q

What is the role of non selective beta blockers in thyrotoxicosis?

A
  • in short term - deals with problems / clinical features of thyrotoxicosis
    e. g tachycardia / tremor
21
Q

why are the beta blockers used NON SELECTIVE?

A
  • so that it reduces all effects of excess stimulation of B-adrenoreceptors
  • cardioselective = only helps with tachycardia - doesn’t help tremor
22
Q

How is Iodide Potassium Iodide given?

when would you give KI to patients?

A
  • given at doses at least 30 x average daily requirement

given in :

  • preparation of surgery of hyperthyroid patients
  • severe thyrotoxic crisis (thyroid storm)
23
Q

Describe the mechanism of action of KI

A
  • by giving lots of KI
  • through wolff chaikoff effect
  • you inhibit iodination of thyroglobulin + generation of H2O2
  • has much quicker effect than giving antithyroid drugs
24
Q

Describe the Wolff chaikoff effect.

A
  • temporary reduction in thyroid hormones following ingestion of large amounts of iodine

Note: Autoregulatory phenomenon

25
Q

How is KI useful for pre surgery?

A
  • reduces size + vascularity of thyroid within couple of weeks
26
Q

What are some unwanted effects of KI?

A
  • allergic reaction

rashes, fever, angio-oedema

27
Q

Describe the pharmacokinetics of KI administration.

A
  • given orally

- max effects after 10 days (continuous administration)

28
Q

What is the effect of radioidine? What does it do?

A
  • treats graves disease
  • treats plummer’s disease
  • treats thyroid cancer
  • switches off thyroid completely
29
Q

What does the effect of radio iodine rely on?

A
  • relies on thyroid gland taking up iodine

- to make thyroid hormone

30
Q

Describe the mechanism of Radioiodine.

A
  • so thyroid follicular cells take up iodine + accumulates in the colloid.
  • from colloid –> emits Beta particles of radiation that destroys follicular cells
31
Q

Describe the pharmacokinetics of radioiodine

A
  • discontinue anti thyroid drugs 7-10 days prior to radioiodine treatment
  • administer as single oral dose
  • has radioactive life of 8 days
  • radioactivity = negligible after 2 months

NOTE:

  • avoid close contact w small children for several weeks
  • contra indicated in pregnancy + BREAST FEEDING

eLCRS - 엔도 (20 decks)

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