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BRS Endocrinology > 1b// Hyperthyroidism > Flashcards

1b// Hyperthyroidism Flashcards

1
Q

Add how a thyroid follicular cell works…

A
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2
Q

How is the thyroid controlled?

A

1) Hypothalamus releases TRH (thyrotropin releasing hormone)

2) Which stimulates the pituitary to release TSH (thyroid stimulating hormone)

3) Which causes the thyroid to release thyroxine (T4) and triiodothyronine (T3)

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3
Q

What level of TSH will you find in a patient with primary hypothyroidism, where the thyroid gland has been destroyed by the immune system?

A

High TSH

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4
Q

When do you know what dose is correct of T4 replacement therapy?

A

Increase the dose until TSH falls to normal

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5
Q

What is Grave’s disease?

A

Autoimmune
Antibodies bind to and stimulate TSh receptor in the thyroid
Cause goitre (smooth and larger) and hyperthyroidism

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6
Q

What are symptoms of Grave’s disease?

A

perspiration
muscle wasting
shortness of breath
breast enlargement
loss of weight
rapid pulse
warm, moist palms
amenorrhea
localized myxedema
(nervousness, excitability, restlessness, insomnia, emotional instability)
Exophthalmos
Palpitation, tachycardia
Increased appetite

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7
Q

What causes exophthalmos in Grave’s disease?

A

Other antibodies bind to muscles behind the eye and cause exophthalmos

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8
Q

What is pre-tibial myxoedema, and when can it be noticed?

A

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

hypertrophy

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9
Q

What causes pre-tibial myxoedema in Grave’s?

A

other antibodies

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10
Q

What is myxoedema?

A

hypothyroidism

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11
Q

What is the antibody involved in Grave’s?

A

TSH-receptor antibody (TRab) (against the TSH receptor)

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12
Q

How do you measure TRab, and when do you do the test for it?

A

in bloodstream during Grave’s disease

it is the first-line investigation to confirm Grave’s

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13
Q

What is toxic nodular thyroid disease?

A

Single toxic nodule/ multiple toxic nodules (multinodule goitre)

NOT autoimmune

Benign adenoma(s) overactive at making thyroxine

No pretibial myxoedema or exophthalmos

Overactive thyroid

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14
Q

What happens to the thyroid gland during toxic nodular thyroid disease?

A

normal gland atrophies because there is no TSH

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15
Q

When does toxic nodular thyroid disease occur age wise?

A

older people, 50-60

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16
Q

What is the effect of thyroxine on the sympathetic nervous system and outcomes of it (4)?

A

Sensitises beta adrenoreceptors to ambient levels of adrenaline and noradrenaline.

Thus there is apparent sympathetic activation.

Tachycardia, palpitations, tremor in hands, lid lag

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17
Q

Symptoms of hyperthyroidism?

A

weight loss (despite increased appetite)
breathlessness
palpitations, tachycardia
sweating
heat intolerance
diarrhoea
lid lag and other sympathetic features

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18
Q

What is a thyroid storm considered medically and why?

A

medical emergency: 50% mortality untreated

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19
Q

What would the blood results from someone with a thyroid storm show?

A

hyperthyroidism

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20
Q

What are symptoms of a thyroid storm?

A

Hyperpyrexia (fever) >41 degrees
Accelerated tachycardia/ arrhythmia
Cardiac failure
Delirium/ frank psychosis
Hepatocellular dysfunction; jaundice

Needs aggressive treatment

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21
Q

What are the treatment options for hyperthyroidism?

A

Drugs
Surgery (thyroidectomy)
Radioiodine

22
Q

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

A
  1. Thionamides (anti-thyroid drugs)
    - propylthiouracil (PTU)
    - carbimazole (CBZ)
  2. Potassium iodide
  3. Radioiodine
  4. Beta blockers
23
Q

What do beta blockers do with regard to hyperthyroidism?

A

help with symptoms

24
Q

What do thionamides, potassium iodide and radioiodine do with regards to hyperthyroidism?

A

Reduce thyroid hormone synthesis

25
Q

What is the use of thionamides?

A

clinical use, daily treatment of hyperthyroid conditions
- grave’s
- toxic thyroid nodule(s) goitre

26
Q

What are the steps involved in thyroid hormone synthesis?

A
  1. TSH attaches to TSH receptor on the basolateral side of the cell
  2. Which then triggers the nucleus to make thyroglobulin
  3. Na+ and I- from the blood enter the cell on the basolateral side by the same ion channel
  4. The TSH-R also causes thyroperoxidase to go across the cell’s apical side into the colloid
  5. iodide ions go through the cell’s apical side via an ion channel
  6. in the colloid iodide ion goes through iodination to become iodine and it then combines with thyroglobulin
  7. this goes through iodination again
  8. this makes thyroglobulin attached to MIT and DIT
  9. via a coupling reaction it makes TG attached to T3 and T4
  10. the thyroglobulin attached to the t3 or t4 is endocytosed and merged with a lysosome
  11. lysosome enzymes cleave thyroglobulin from t3 and t4
  12. hormones diffuse into bloodstream
27
Q

What are the overall 4 steps of thyroid hormone synthesis?

A
  1. uptake of iodide by active transport
  2. iodination
  3. coupling reaction: storage in colloid
  4. endocytosis and secretion
28
Q

What is the mechanism of action of thionamides?

A

inhibition of thyroid peroxidase and hence t3/4 synthesis and secretion

29
Q

How long does the biochemical effect of thionamides last?

A

hours

30
Q

How long does the clinical effect of thionamides last?

A

weeks

31
Q

What may thionamides treatment regimen include and what does it do?

A

propranolol

rapidly reduces tremor and tachycardia

32
Q

What are unwanted actions of thionamides?

A

agranulocytosis (reduction in neutrophils)- rare and reversible on withdrawal of drug
- that’s why if you are put on it and feel something and feel smth for the 24hr u are on it you go straight to a and e

rashes- relatively common

33
Q

What is the follow up to anti-thyroid drugs?

A

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

only cures 50% of patients, the rest either have surgery or life of carbimazole

review of patient periodically including thyroid function tests for remission/ relapse

34
Q

What is the role for b blockers in thyrotoxicosis?

A

several weeks for ATDs to have clinical effect e.g., reduced tremor, slower heart rate, less anxiety

non-selective (I.e., B1 and B2) blocker e.g., propranolol achieves these effects in the interim

35
Q

how is iodide usually given to patients and how high is the dose?

A

usually potassium iodide (doses at least 30x the average daily requirement)

36
Q

Why is potassium iodide used for hyperthyroid patients?

A
  • preparation for surgery
  • during a severe thyrotoxic crisis (thyroid storm)
  • treat severe hyperthyroidism
37
Q

What is the mechanism of action for KI?

A
  1. inhibits iodination of thyroglobulin
  2. inhibits H2O2 generation + thyroperoxidase
38
Q
A
39
Q

What is the name of the effect that KI causes?

A

Wolff-Chaikoff effect

40
Q

What is the Wolff-Chaikoff effect?

A

inhibition of thyroid hormone synthesis and secretion
- presumed autoregulatory effect

an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones

41
Q

How long after taking KI does the hyperthyroidism symptoms reduce?

A

reduce within 1-2 days

42
Q

How long does it take for the thyroid gland to reduce size after taking KI?

A

10-14 days

43
Q

How would you describe a hyperplastic thyroid gland and the cells in the gland?

A

gland enlarged
red (engorged)
tears easily
bleeds readily

acinar hyperplasia and loss of colloid

44
Q

How would you describe a hyperplastic thyroid gland after thiouracil and the cells in the gland?

A

gland mass further increases
more engorged
tears more easily
bleeds more readily

increase in acinar hyperplasia
complete loss of colloid

45
Q

How would you describe a hyperplastic thyroid gland after thiouracil and iodide and the cells in the gland?

A

gland reduced in size
pale and firm
does not tear and bleed so readily

involution of acinar epithelium
storage of iodine-poor colloid
mean cell height is much smaller

46
Q

What are problems with thyroid surgery?

A

risk of voice change (recurrent laryngeal nerve)

risk of also losing parathyroid glands (reliant on calcium)

scar

anaesthetic

47
Q

When can you not take radioiodine?

A

during pregnancy

48
Q

What is a precaution you must do for others if you have taken radioiodine?

A

avoid children and pregnant women for a few days (due to radiation)

49
Q

Why do you take radioiodine?

A

for scans only, not treatment, 99-Tc

50
Q

What is an example of a radioiodine?

A

99-Tc pertechnetate (an iodine isotope)

all radioiodines are iodine isotopes

51
Q

What are treatment options for hyperthyroidism?

A

Drugs:
beta blockade is very important
- propranolol is beta blocker example and main option

anti-thyroid drugs:
carbimazole
propylthiouracil

52
Q
A

BRS Endocrinology (12 decks)

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