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Year 2 LCRS Endocrinology > Thyroid > Flashcards

Flashcards in Thyroid Deck (30)
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1
Q

Which effects has TSH on the thyroid gland?

A

It binds to the Thyroid receptor and

  1. mediates iodine intake into colloid
  2. meditaes release of already formed T3/T4
2
Q

Recall the symptoms of Myxoedema

A

Low basal rate resulting in

  • tiredness
  • depression
  • cold intolerance
  • weight gain
  • constipation
  • bradycardia

–> in severe cases: might lead to myxoedema coma!

3
Q

What is the cause of myxodema?

A

Prymary hypothyroidism due to autoimmune response on thyroid

4
Q

What are the biochemical features of Myxodema?

A

High TSH

Low T3/T4

5
Q

How would you treat somone with hypothyroidism?

How are the right dosages adjusted?

A

Usually T4 replacement (Levothyroxine sodium)

  • T4= prohormone that is converted into active T3 by enzymes in body
  • In primary hypothyroidism: TSH levels are used to adjust dosage
  • In secondary hypothyroidism: free T4 (normally 99.7% bound to Thyroid binding globulin) middle-range levels are aimed

T3 replacement Liothyronine sodium

  • less commonly used: normally only used as IV shot when myxodema come –> faster action
6
Q

What are the advantages and limitations of T3 replacement or a combined replacement instead of T4 replacement in hypothyroidism?

A

No evidence-based advantages known

  • it is more expensive
  • As T3 is active form: higher risk of toxicity leading to hyperthyrpoid symptoms like:
    • palpitations, tremor, anxiety - often combination treatment suppresses TSH
7
Q

How are thyroid hormones transported in blood?

Why is this important to consider when supplementing the hormones

A

It is highly bound to Thyroxine binding globulin (TBG) –> 99.7% T4 is bound, 99.97% T3 bound

BUT: TBG levels can differ:

  • plasma binding proteins increase in pregnancy and on prolonged treatment with oestrogens and phenothiazines
  • TBG falls with malnutrition, liver disease
  • certain co-administered drugs (e.g. phenytoin, salicylates) compete for protein binding sites.
8
Q

What is the prefered route of administration of thyroid hormones?

What is their half-life?

A
  1. active orally –> tablet
  2. Half-life long
  • Levothyroxine (T4) plasma half life of 6 days
  • Liothyronine (T3) plasma half life 2.5 days

–> Not the end of the world when somone forgets to take one tablet etc.

9
Q

What are the three targets of the different Antibodies in Grave’s disease?

Which symptoms do they cause?

A
  1. Antibodies binding to TSH receptors
    • Hyperthyroidism
  2. Antibodies binding to GH receptor at back of eye
    • Exophtalamos –> starring appearance, can’t close eye
  3. Antibodies binding to GH receptors at ancles
    • Pretibial myxedema –> not pitting-oedema due to growth of soft tissue
10
Q

What happens to the ß-Receptors in Grave’s disease?

A

ß-receptors are more sensitive to adrenaline –>increased SNS reaction

11
Q

How does the thyroid in someone with Graves’ disease feel on examination?

A

Symmetrical

Smooth

Enlarged (goiture)

Moves when swallowing (indication that it is thyroid)

Not painful on examination

12
Q

What is Plummers disease?

A

Benign adenoma that is overactive at making thyroxine

13
Q

What would a thyroid in someone with Plummer’s disease on examination look/feel like?

A

Toxic nodular goiture

Asymmetrically enlarged (tumor)

not painful

On scintigram:

  • “hot nodule”,
14
Q

What is lid lag?

When and why does this symptoms occur?

A

When lowering the eyes:

Normally: there is no white in the eye seen above the iris (because eye lid follows eye movement)

In Lid lag:

  • White above the eye can be seen when lowering the eyes because eye lid reaction is delayed
  • Because of increased sympathetic reaction of the eyelid (that pulls it back) due to an increased sensitivity of ß receptors due to hyperthyroidism
15
Q

What is a thyroid storm?

A

Very rare: but 50% mortality (due to arrythmias and heart failure)

–> Hyperthyroidism

body temperature, heart rate, blood pressures are dangerously high

16
Q

What are the symptoms of a thyroid storm?

A
  • Hyperpyrexia (>41°)
  • tachycardia, arrythmia
  • cardia failure
  • delirium/frank psychosis
  • hepatocellular disfunction –> jaundice

–> if someone with hyperthyroidism has 2 or more symptoms –> immediate, agressive treatment

17
Q

What is pyresia?

A

Fever

18
Q

What is ESR? What do the test results show?

A

ESR= Erythrocyte Sedimentation Rate

how fast erythrocytes settle down

–> faster in inflammation

19
Q

What are the symptoms of viral thyroiditis?

How would the thyroid feel on examination?

A
  • •Painful dysphagia
  • •Hyperthyroidism
  • •Pyrexia
  • •Raised ESR

Examinaiton

  • enlarged, asymetrically
  • tender (painful on palpation)
20
Q

What happens during a viral thyroiditis?

How does this lead to hyperthyroidism?

A
  • Virus attacks thyroid gland causing pain and tenderness
  • Thyroid stops making thyroxine and makes viruses instead
  • Thus no iodine uptake (ZERO)

BUT: Stored thyroid hormones are released causing hyperthyroidism

–> but 4 weeks after thyroidits: hypothyroidism (stored emptied)

–> after a further month: euthyrooid (stores filled up, normal function)

21
Q

Explain the use and function of a technetium scan

A

Tyroid takes Technetium (Tc 43) up (instead of iodine) (rather radioactive isotop: Tc-99m)

–> can be seen on scans (radioactive radiation detected)

22
Q

What is chemosis?

A

Red/sore eyes (oedema of conjunctiva)

–> non-specific sign to irritation

23
Q

What is the usual treatment for someone diagnosed with Graves’ disease?

A
  1. Daily treament with thionamides (thiourylenes; anti-thyroid drugs)
  2. At begining: togehter with non-selective ß-blockers to manage symptoms
  3. Usually aimed to stop anti-thyroid drug treatment after 18 months

Review patient periodically including thyroid function tests for remission/relapse

24
Q

What are the aniti-thyroid drugs used in hyperthyroidism?

What is their mechanism of action?

A

I.e. daily treament for Gaves’ and Toxic thyroid nodule/toxic multinodular goitre

  1. propylthiouracil (PTU)
  2. carbimazole (CBZ)

–>

  1. Inhibits production and secretion of T3/T4 (by inhibiting thyroid peroxidase)
  2. May reduce production of antibodies in Graves’
  3. And PTU reduces conversion of T4 into T3 in peripheral tissues
25
Q

What are the side effect of anti-thyroid drugs?
Why is this important when prescribing these medications?

A

Safe drug but:

Agranulocytosis (usually reduction in neutrophils) - rare and reversible on withdrawal of drug.

–> Need to tell patients to come in when having a cold, raised temp. etc. to do full blood count

·rashes (relatively common)

26
Q

Explain the administration and metabolism of Carbimazole

A

i) orally active
ii) carbimazole is a pro-drug which first has to be converted to methimazole
iii) cross placenta, secreted in breastmilk (preferred PTU in pregnancy)

–> try to avoid during pregnancy and breastfeeding

iv) metabolised in liver and excreted in urine

27
Q

Which drug is administered together with anti-thyroid drugs in hyperthyroidism to manage the symptoms?

What is its’ major contraindication?

A

Non-selective ß-blockers

  • Anti-thyroid drugs need several weeks till effect–>reduced tremor, slower heart rate, less anxiety
  • propranolol (non-selective ß blocker) to help with symptoms (connected to hyersensitivity to adrenaline)
  • Not for astmatics!
28
Q

Explain the use of Iodine in the treatment of hyperthyroidism

A

Indications

  • Prep for surgery (want less SNS when surgery)
  • Thyroid storm

–> need to be taken out afterwards (because expected later high levels of thyroid hormones)

Administraion

  • Usually KI
  • Orally (maximal effects after 10d of continous administration
  • inhibits H2O2 formation and thyroid peroxidase effect and ionidation of tyhoroglobulin

Induced the Wolff-Chaikoff effect:

  • presumed autoregulatory effect
  • no secretion of thyroid hormone after large dose of iodine –> fast reaction (withing 1-2 days)

Side effects

  • allergic reactions
29
Q

Explain the use of Radioiodine in the treatment of Hyperthyroidism

A

Radioactive Iodine administration (single oral dose)

  • is being taken up by thyroid
  • ß-radiation destroys thyroid (half life 8 days, radiation after 2 month neglectible)
  • After that: replacement with T4 (TSH levels used to find dose)

Cautions

  • ·Avoid close contact with small children for several weeks after receiving radioiodine.
  • ·Contra-indicated in pregnancy and breast feeding
  • Might need some days off work
30
Q

What are the side effects/risk of a thyroidectomy?

A

Hoarse voice: damage to recurrent laryngeal nerve

Risk of hypoparathyroidism after thyroidectomy (is difficult to treat)