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Year 2 - Endocrinology > Hyperthyroidism & Disorders > Flashcards

Hyperthyroidism & Disorders Flashcards

1
Q

2 potential causes of hyperthyroidism?

A

Graves’ disease

Plummer’s disease (nodular goitre)

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2
Q

What is the difference between the 2 potential causes of hyperthyroidism?

A

Graves’ disease - autoimmune!
Abs bind to & stimulate TSH receptors in the thyroid gland

Plummer’s disease - NOT autoimmune - due to benign adenoma

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3
Q

Link between autoimmune & thyroid diseases?

A

Can cause BOTH HYPO and HYPER thyroidism

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4
Q

What does Graves’ disease cause?

A

x Goitre (smooth!) - thyroid gland grows
x Hyperthyroidism
x Lid lag
x Exophthalmos - Abs bind to muscles behind the eye = bulging
x Pretibial myxoedema (hypertrophy) - growth of soft tissue on the shins! (non-pitting!!)

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5
Q

What causes lid lag?

A

In Graves’s Disease

2 nerves open the eye (one is under SN control) - thyroxine makes the beta adrenoceptors more sensitive to adrenaline which causes the eyelid to open/be pulled back

Leads to apparent SNS activation - tachycardia, lid lag, palpitations etc.

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6
Q

3 things the Abs cause in Graves’ Disease?

A

x Goitre
x Exophthalmos
x Pretibial myxoedema

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7
Q

2 parts to exophthalmos?

A
  1. Eye lid is OPEN due to the thyroxine-causing adrenaline (lid lag)
  2. Eyeball is pushed forward due to the GFs in the Abs
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8
Q

What causes a smooth goitre?

A

Graves’ Disease

Abs bind to the TSH receptors on the follicular cells - makes them work harder & GROW SMOOTHLY!

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9
Q

How can Graves’ Disease be seen in a scan?

A

Radioactive iodine given and scan!

WHOLE gland is overactive as Abs bind to all gland (OneNote!!)

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10
Q

What does Plummer’s disease cause?

A

x TOXIC NODULAR goitre (NOT smooth!)

x Benign adenoma - overactive at making thyroxine

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11
Q

Difference between Graves’ and Plummer’s Disease?

A

Plummer’s Disease:
x NO pretibial myxoedema
x NO exophthalmos
x Goitre is a toxic nodular

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12
Q

Signs & symptoms of GENERAL hyperthyroidism?

A 
x Weight loss
x Increased appetite
x Palpitations
x Tachycardia
x Sweating/Palpitations
x Heat intolerance
x Diarrhoea
x Lid Lag
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13
Q

How can Plummer’s Disease be diagnosed?

A

Will NOT feel a smoothly enlarged goitre:

  • One clone of follicular cells grow to form the tumour
  • All the follicular cells then make thyroxine
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14
Q

How can Plummer’s Disease be seen in a scan?

A

In radioactive iodine scan, will see part of the thyroid gland as tumour!

Normal thyroid gland becomes SMALLER as the PG STOPS making TSH (-ve feedback!)

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15
Q

Another name for Plummer’s Disease as not used as much anymore?

A

Nodular Goitre (‘Hot nodule’)

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16
Q

Link between thyroxine & SN?

A

Sensitive beta adrenoceptors to levels of A & NA

So apparent SN activation - tachycardia, palpitations, tremor in hands, lid lag etc

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17
Q

What is a thyroid storm?

A

It is a medical emergency (50% mortality is untreated)

Blood results confirm hyperthyroidism

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18
Q

Features of thyroid storm?

A 
x Hyperpyrexia (high fever) > 41oC
x Accelerated tachycardia/arrhythmia
x Cardiac failure
x Delirium/frank psychosis
x Hepatocellular dysfunction - e.g. jaundice
19
Q

Treatment for thyroid storm?

A

Needs AGGRESSIVE treatment:

  • Surgery (thyroidectomy)
  • Radioiodine
  • Drugs
20
Q

4 types of drugs used in the treatment of hyperthyroidism?

A
  1. Thionamides (thiourylenes; anti-thyroid drugs)
  2. Potassium Iodide
  3. Radioiodine
  4. Beta-blockers
21
Q

2 specific thionamides (drugs)?

A 
x Propylthiouracil (PTU)
x Carbimazola (CBZ)
22
Q

What do each of the drugs do?

A

x Thionamides, Potassium Iodide & Radioiodine - REDUCE thyroid hormone synthesis

x Beta-blockers - help with SYMPTOMS

23
Q

What is the potential clinical use of thionamides?

A
  1. Daily treatment of hyperthyroid conditions (e.g. Graves’ & Nodular Goitre)
  2. Treatment prior to surgery
  3. Reduction of symptoms (while waiting for RADIOACTIVE IODINE to act!)
24
Q

What is the mechanism of action of thionamides?

A
  1. Inhibit TPO (thyroid peroxidase) = reduce T3/T4 synthesis & secretion
  2. Supress Ab production in Graves’
  3. Reduce CONVERSION (deiodination) of T4 –> T3 in peripheral tissyes (PTU)
25
Q

Difference in biochemical & clinical effect of thionamides?

A

Biochemical effects - HOURS

Clinical effects - WEEKS

26
Q

Why is there a difference in biochemical & clinical effect of thionamides?

A

As there is a large store of thyroxine in the thyroid gland already which is released for a while SO chemical effects takes WEEKS to show

27
Q

What else may be given with thionamides in the treatment regimen and why?

A

Propranolol! (beta-blocker)

Rapidly reduces termor & tachycardia

28
Q

Unwanted actions associated with thionamides?

A

x Agranulocytosis (usually reduction in neutrophils) - rare & reversible on drug withdrawal

x Rashes - relatively common

29
Q

Pharmacokinetics associated with thionamides?

A

i) orally active
ii) CBZ is a PRO-DRUG - must first be converted to methimazole
iii) Can cross the placenta as secreted in breastmilk (CBZ more so than PTU)
iv) Metabolised in the liver & secreted in urine
v) Plasma half-life of 6-15 hours

30
Q

Follow-up of treatment associated with thionamides?

A

Usually aim to stop treatment after 18 months - propranolol also ceased when drug is in full effect

Patient is reviewed periodically - includes thyroid function tests for remission/relapse

31
Q

Why is a NON-selective beta-blocker preferred for thyrotoxicosis?

A

WANT the wide-spread affects as want reduced tremor, slower HR, less anxiety etc. in the intermin

Have this less so with selective beta-1 blockers e.g. atenolol

32
Q

What is the potential clinical use of Iodide treatment (KI)?

A
  • Preparation of hyperthyroid patients for surgery
  • In severe thyrotoxic crisis (THYROID STORM!)

Dosage at least 30X the average daily requirement

33
Q

What is the MOA of Iodide treatment (KI)?

A
  1. Inhibits iodination of thyroglobulin (TG)

2. Inhibits H2O2 (hydrogen peroxide) generation

34
Q

What does the MOA achieve in Iodide treatment (KI)?

A

Inhibition of T.H synthesis & secretion = WOLFF-CHAIKOFF EFFECT (presumed auto-regulatory effect)

x Hyperthyroid symptoms reduce within 1-2 days
x Vascularity and size of gland reduces within 10-14 days (very helpful for Graves’ if going into surgery)

35
Q

Unwanted actions associated with Iodide (KI)?

A

Allergic reaction e.g. rashes, fever, angio-oedema

36
Q

Pharmacokinetics actions associated with Iodide (KI)?

A

x Orally active - Lugol’s solution / Aq iodide

37
Q

When is the maximum effect seen with Iodide (KI) treatment?

A

After 10 days of CONTINOUS administration

38
Q

What is the potential clinical use of Radioiodine (I131)?

A

x Hyperthyroidism (Graves’, nodular goitre)

x Thyroid cancers

39
Q

When can patients plan to use Radioiodine?

A
  • If don’t want to be on long-term ATDs (e.g. if thinking about pregnancy)
  • Or is ATD is not working as difficult to control
40
Q

What is the MOA of radioiodine treatment (KI)?

A

Given in HIGH doses!

RadioIODINE accumulates in colloid and emits beta-particles = destroys follicular cells

41
Q

Pharmacokinetics actions associated with radioiodine?

A
  • Discontinue ATDs 7-10 drugs prior to treatment - so can be taken up by thyroid as much as possible
  • Administer as SINGLE ORAL dose
    x Graves’ - approx 500 MBq
    x Cancer - approx 3000 MBq
  • Radioactive half-life of 8 days
  • Radioactivity negligible after 2 months
42
Q

Cautions associated with radioiodine?

A
  • Avoid close contact with small children for several weeks after receiving treatment
  • CONTA-indicated in pregnancy and breast-feeding
43
Q

Essentially, what is achieved after radioiodine treatment?

A
  1. Switches OFF the thyroid gland for good
  2. Thyroxine falls
  3. TSH starts to rise
  4. Start patients on thyroxine - daily doses!
44
Q

What else can given as radioiodine?

A

Radioiodine - HIGH doses

Technetium 99 pertechnetate - LOW dose traver

Year 2 - Endocrinology (19 decks)

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