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Y2 LCRS 1 - Endocrinology > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

State two common causes of hyperthyroidism.

A

Graves’ Disease

Plummer’s Disease (nodular goitre)

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2
Q

What type of disease is Graves’? Describe its mechanism.

A

AUTOIMMUNE DISEASE

  • The body produces an antibody that behaves like TSH
  • The antibody binds to the TSH receptor on the thyroid gland stimulating it to produce thyroid hormones
  • The antibody is constantly stimulating the thyroid gland, leading to excessive hormone production
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3
Q

What does a thyroid gland look like in Graves’ Disease?

A

The whole thyroid gland is smoothly enlarged and the whole gland is active → smooth goitre

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4
Q

State some features of hyperthyroidism.

A

Increased BMR so everything speeds up

  • Weight loss despite increased appetite -
  • Breathlessness
  • Tachycardia and palpitations
  • Heat intolerance (always feeling hot) → sweating
  • Diarrhoea - bowel speeds up
  • Oligomenorrhoea/amenorrhoea
    • Lack of body fat tells the brain that it is not a good time to reproduce as the body lacks resources
    • Therefore, the brain shuts down the reproductive axis
  • Sympathetic features:
    • Lid lag (delay in movement of the eyelid as the eye moves downwards so you can see the whites of the eyes above the iris - ABNORMAL)
    • Tachycardia and palpitations (suddenly noticeable heartbeat - usually rapid, strong or irregular)
    • Tremor in hands - motor nerve terminals to skeletal muscle have adrenergic receptors which stimulate ACh release at the NMJ, so excessive activation can cause tremors (involuntary muscle contractions)
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5
Q

What are two defining features of Graves’ and what is it caused by?

A
  • Pretibial myxoedema
    • Antibodies bind to fibroblasts in the skin and stimulate them to produce excessive glycosaminoglycans leading to swelling
  • Exophthalmos
    • Abnormal protrusion of the eyeball (bulging eyes)
    • Antibodies bind to muscles behind the eye (exrtaocular muscles) leading to swelling behind the eyes, pushing the eyeballs forward → inflammatory process

These are defining features of Graves becuase they are both caused by antibodies (i.e. autoimmune disease)

  • These antibodies which bind to the TSH receptor also bind to other simialr structures (receptors), leading to these other symptoms
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6
Q

Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.

A

The whole of the thryroid gland would take up the radioactive iodine and would show up on the scan

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7
Q

What causes Plummer’s Disease?

A

It is caused by a benign adenoma in the thyroid gland

These tumour cells are overactive at making thyroxine (i.e. produce thyroxine independent of TSH)

  • NOTE:
    • Tumours arise due to mutations in cell cycle Regulation, so they are abnormal anyway
    • therefore, these mutations could also have made them less sensitive to endogenous mechanism used to regulate thyroid hormone production
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8
Q

How does Plummer’s disease differ from Graves’?

A

It is NOT autoimmune therefore:

  • NO pretibial myxoedema
  • NO exophthalmo

You get a toxic nodular goitre - i.e. the benign adenoma is the toxic nodule

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9
Q

What will a technetium or radioactive iodine scan of the thyroid show in a patient with Plummer’s Disease?

A

All the iodine will be taken up by the overactive, tumorous part of the thyroid so you will see a hot nodule appear

The rest of the thyroid gland will not be seen because:

  • The high thyroxine production will decrease TSH release from the anterior pituitary
  • Therefore, no TSH to stimulate the rest the rest of the thyroid gland to produce any thyroxine
  • If it is not producing thyroxine, then it will not need to take up the iodine

NOTE: Technetium (Technetium 99 Pertechnetate) is a radioactive element and is used more often in thryroid scans nowadays instead of radioactive iodine, because it mimics the effects of iodine (i.e. taken up in same way) BUT involves a lower radiation dose and is cheaper

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10
Q

Describe the effects of thyroxine on the sympathetic nervous system.

A

Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline

  • The levels of adrenaline and NA in the body don’t change
  • But the adrenoreceptors become more sensitive to adrenaline and noradrenaline
  • Therefore, with the same amounts of hormone, you get a stronger response → symptoms of having high adrenaline/NA
  • NOTE: thyroxine (once converted to T3) works by increasing the number of beta adrenorecptors
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11
Q

What is thyroid storm (thyrotoxic crisis) and what are the features of thyroid storm?

A

This is a medical emergency that is a rare but important complication of hyperthyroidism

Diagnosis:

  1. Blood test to confirm hypothyroidism
  2. Any two of these features present (due to extremely high thyroid hormone levels):
    • Hyperpyrexia (very high fever - body temp > 41°C)
    • Accelerated tachycardia/arrhythmia
    • Cardiac failure - following sudden increase in BP
    • Delirium/frank psychosis (hallucinations, delusions)
    • Hepatocellular dysfunction; jaundice - thyroid hormones maintain the metabolism of bilirubin
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12
Q

State four treatments for hyperthyroidism.

A
  • Thionamides
  • Potassium Iodide
  • Radioiodine
  • Beta Blockers

NOTE: First 3 drugs recuce thryroid hormone synthesis; beta blockers only relieve symptoms

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13
Q

State two thionamides.

A

Propylthiouracil (PTU)

Carbimazole (CBZ)

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14
Q

What are thionamides used to treat and when would you use it?

A

Used to treat:

  • Graves’ Disease
  • Plummer’s Disease

How it’s used clinically:

  • Given daily and orally active (i.e. taken orally)
  • Before thyroidectomy to stabilise the patient
    • You wouldn’t want to give general anaesthetic to someone who is has tachycardia - tachycardia while unconscious is dangerous
  • It can be used after radioiodine treatment while you’re waiting for the clinical effects of the treatment
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15
Q

Describe the synthesis of thyroxine by follicular cells.

A
  • Thyroglobulin (prohormone) is a protein produced by the follicular cells and stored the colloid
  • Active uptake: Iodine is actively taken up from the blood by the follicular cells and into the colloid
  • Iodination: In the colloid, thyroid peroxidase (TPO), in the presence of hydrogen peroxide iodinates the tyrosyl residues on the thyroglobulin to produce monoiodotyrosine (MIT) or diiodotyrosine (DIT)
  • Coupling reactions: Peroxidase transaminase or TPO then couples MIT and DIT to form T3 and T4, which is stored in the colloid (when stored then T3 and T4 still attached to thryroglobulin)
  • Endocytosis and secretion: T3 and T4 endocytosed into follicular cell and fuses with a lysosome containing enzymes which break down the thyroglobulin protein, liberating T3 and T4 which are then secreted into the circulation
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16
Q

What is the mechanism of action of thionamides?

A

Thionamides inhibit thyroid peroxidase

  • This prevents the iodination of thyroglobulin and coupling of MIT and DIT
  • This results in reduced synthesis and therefore secretion of T3 and T4
17
Q

Why do thionamides have a delayed effect on thyroid hormone levels?

A

Thionamides are quick in inhibiting synthesis of thyroid hormone (i.e. fast biochemical effect)

BUT the clinical effect (i.e. symptomatic relief) is longer becuase the thyroid hormones which have been already synthesised and are stored in the colloid will still be released and cause symptoms

  • Large amount of stored hormones due to overactive thyroid gland

The result is a big delay between the biochemical effects (hours) and the clinical effects (weeks)

18
Q

What would you give the patient temporarily whilst waiting for thethionamides to have their clinical effect?

A

Non-selective beta-blockers (i.e. targets beta 1 AND beta 2 receptors)

  • This will reduce the effects of beta sensitisation by thyroxine
  • Therefore will help relieve sympathetic symptoms such as tremor, tachycardia, palpitations, anxiety etc.
  • Example drug used: propanolol

NOTE: Using propanolol is preferred over beta 1 selective beta blocker (e.g. atenolol) at relieving symptoms and improving overall wellbeing

19
Q

What are the other mechanisms of action of thionamides (other than thyroid peroxidase inhibition - main)?

A
  • May suppress antibody production in Graves’ - as thianomides have immunosupressive properties
  • PTU: Reduces deiodination of T4 to T3 in peripheral (target) tissues
20
Q

State some unwanted effects of thionamides.

A
  • Agranulocytosis/granulocytopenia (rare and reversible with withdrawal of the drug)
    • Body doesn’t make enough granulocytes - agranulocytosis
    • This leads to a severe reduction of granulocytes (neutrophils, basophils, eosinophils) in the bloodstream - granulocytopenia
  • Rashes (relatively common)
21
Q

Carbimazole is a pro-drug. What is it converted to become active?

A

Methimazole

22
Q

What are the implications of thionamides in pregnancy?

A

Thionamides can cross the placenta and is present in breast milk so it can cause foetal hypothyroidism

  • This means that you would want to give as low a dose as possible to a patient who is trying to conceive and is taking thionamides
  • PTU does this less than CBZ (in term of crossing the placenta and being secreted into breastmilk)

Thionamides are metabolised in the liver and excreted in the urine

23
Q

What is the follow-up procedure for a patient taking anti-thyroi drugs (i.e. thionamides)?

A
  • Usually aim to stop anti-thyroid drug treatment after 18 months
  • Review patient periodically including thyroid function tests for remission (disappearing of symptoms) or relapse
24
Q

What is the mechanism of action of iodide (usually KI) treatment?

A
  • Normally iodine stimulates thyroid hormone synthesis
    • Hormones formed by iodination of thyroglobulin (protein pro-hormone)
  • However, If you give a massive dose of iodine (at least 30 times the average daily requirement) it can inhibit thyroid hormone synthseis and secretion
    • This is the Wolff-Chaikoff effect
  • ​Mechanisms of inhibition:
    • Inhibits H2O2 generation and thyroid peroxidase action
    • Inhibits iodination of thyroglobulin
      • H2O2 generation in the thyroid gland is necessary for TPO action as it is a co-substrate in the reaction described below
      • H2O2 used to oxidise iodine - i.e. convert it into a reactive form so it can then iodinate thyroglobulin
  • This treatment is effective - hyperthyroid symptoms

reduce within 1-2 days

25
Q

What is the Wolff-Chaikoff effect?

A

The temporary reduction in thyroid hormones following ingestion of a large amount of iodine

This is presumed to be an autoregulatory effect - i.e. stops body from using all that excess iodine to make too much thyroid hormone

26
Q

Why is potassium iodide useful before surgery?

A

It reduces the size and vascularity of the thyroid gland within 10-14 days

  • If thyroid gland function is inhibited, it doesn’t need as much blood supply
  • The shrrinking of the gland is maybe due to reduction in cell number as not as many cells required during times of reduced function)
27
Q

State some unwanted actions of potassium iodide.

A

Allergic reaction - triggers symptoms like:

  • Rashes
  • Fever
  • Angio-oedema = swelling underneath the skin due to leakage of plasma
28
Q

In what form is potassium iodide given?

A

Lugol’s Solution = aqueous iodine (solution of KI and iodine in water)

  • Taken orally
29
Q

What is radioiodine use to treat?

A

Used to treat:

  • Graves’ Disease
  • Plummer’s Disease (also known as toxic nodular disease)
  • Thyroid Cancer
30
Q

Describe the mechanism of action of radioiodine.

A

High doses of radioactive iodine (I-131) is are used

  • Radioiodine is taken up by the thyroid gland and it accumulates in the colloid
  • From the colloid it emits beta particles that destroy the follicular cells
    • The beta particles essentially damage the DNA in cells (cause breakages in bonds when they collide with the DNA)
    • Due to the extent of the DNA damage, this could induces apoptosis in the cells or cause cell death due to the cell not being able to produce essential proteins needed for survival

NOTE: This is different from using radioactive iodine for the throid scan because that is a much lower radiation dose so very low risk of mutations

31
Q

What do you have to do once the patient has undergone radioiodine treatment?

A

You have to give them thryroxine replacement

  • Since their thyroid gland has been destroyed and can’t produce their own thyroid hormones, they essentially have hypothyroidism
32
Q

Describe the pharmacokinetics of radioiodine.

A
  • It is given orally as a single dose
    • NOTE: higher dose needed to treat thryroid cancer than hyperthryroidism due to fast dividing cells in cancer
  • Discontinue anti-thyroid drugs 7-10 days before radioiodine treatment
    • This is done to allow time for the thyroid gland to become really active again so that it takes up a lot of the radioiodine (to use it to produce thyroid hormone
  • Radioactive half life of 8 days
  • Radioactivity is negligible after 2 months
33
Q

What are some cautions of radioiodine?

A
  • Avoid close contact with small children for several weeks after receiving radioiodine
    • Because the radioactive iodine spreads through the body and is emitted from the body for several weeks due to its fairly long half life
    • Not a high dose of radioactivity because it has diffused through the body but children are more vulnerable so should be kept away
  • Contra-indicated in pregnancy and breast feeding -
    • i.e. should not be used in these situations as the radiation could spread to the baby
34
Q

State some symptoms of viral thyroiditis (de Quervain’s thyroiditis).

A

Painful dysphagia (difficulty swallowing)

Pyrexia (fever = increased body temperature to make it harder for pathogens to survive)

Hyperthyroidism

Raised ESR (eythrocyte sedimentation rate → increases with inflammation)

35
Q

Describe how viral thyroiditis causes hyperthyroid effects.

A

The virus takes over the function of the thyroid and makes the thyroid produce more virus particles rather than producing thyroid hormone - i.e. the thyroid gland stops making thryroid hormones during the infection

It damages the thyroid follicles so that all the T3 and T4 (produced and stored in the follicles) gets released

Though the virus is stopping the production of thyroid hormone, the patient actually presents with hyperthyroid symptoms during the course of the infection because of the release of stored thyroid hormone

36
Q

What is the appearance of a thyroid scan (with raioactive iodine) in a patient with viral thyroiditis?

A

It is not visible in the scan

  • No thryoid hormones being synthesised by the thryroid gland so the thryoid gland is not taking up any iodine
37
Q

Describe the course of action and progression of viral thyroiditis from the time of presentation with hyperthyroid symptoms.

A

Course of action: As it is a viral infection, you just wait for the immune system to get rid of the virus (clear the infection)

Progression:

  • Four weeks after the start of the infectin, all the stored thyroxine in the thryroid gland will run out → patient will have hypothyroid symptoms
  • After another month the cells would have recovered and will start to produce thyroxine again so it will return to normal (euthyroid)

Y2 LCRS 1 - Endocrinology (20 decks)

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