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LCRS Endo > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

what is Grave’s Disease?

A

autoimmune stimulation of TSH receptors in thyroid gland (by antibodies)

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2
Q

how does goitre in graves look like?

A

smooth, symmetrical enlargement

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3
Q

what is lid lag?

what is the mechanism behind this?

A

delay of eyelid when following the pupil

thyroxine sensitises beta adrenoreceptors to ambient levels of adrenaline and noradrenaline (not more adrenaline, but increases sensitivity of receptors)

SNS activation is slowed down in the oculomotor nerve so the eyelid lags

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4
Q

what is the cause of exophthalmos?

A

antibodies attack muscles behind the eyes

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5
Q

what is pretibial myxoedema?

A

growth of soft tissue in shins due to other antibodies

non-pitting, solid oedema

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6
Q

what is the difference between Plummer’s and Grave’s?

A

Plummer’s is not autoimmune
No exopthalamos shown
No pretibial myxoedema

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7
Q

what is Nodular Goitre?

A

aka Plummers

  • not autoimmune
  • benign adenoma causing toxic nodular goitre secreting T4
  • NO pretibial myxoedema
  • NO exophthalamos

produces “hot nodules” on thyroid uptake scan (toxic multinodular goitre)

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8
Q

what are the signs and symptoms of general hyperthyroidism?

A
  • weight loss, increased appetite
  • sweating
  • tachycardia
  • palpitations
  • diarrhoea (overactive bowels)
  • lid lag
  • dyspnoea
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9
Q

Viral thyroiditis as a cause of hyperthyroidism

A
  • de Quervain’s thyroiditis is of viral orgin

- causes hyperthyroidism but eventually lead to hypothyroidism

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10
Q

what are the symptoms of thyroiditis?

A
  • painful/tender dysphagia: viral attack of gland
  • hyperthyroidism
  • pyrexia (fever)
  • raised erythrocyte sedimentation rate
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11
Q

what causes the eventual hypothyroidism in viral thyroiditis?

A

the virus lyse the thyroid cells causing a release in thyroxine into the blood (hyperthyroidism)
thyroid doe not create more thyroxine leading to hypothyroidism after a month

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12
Q

how much uptake is seen on the scan for thyroiditis?

A

zero uptake

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13
Q

what is a thyroid storm?

A

medical emergency with 50% mortality

requires aggressive treatment of surgery, radio iodine and drugs

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14
Q

what are the features of thyroid storm?

A
  • hyperpyrexia (>41 degrees)
  • accelerated tachycardia/arrhythmia
  • cardiac failure
  • delirium/ frank psychosis
  • heptacellular dysfunction, jaundice
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15
Q

what are the 4 classes of drugs used to treat hyperthyroidism?

A

1) thionamides
2) potassium iodide
3) radioiodine
4) beta blockers (symptom treatment)

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16
Q

what is thionamide?

A

affects thyroxine synthesis by preventing iodination of tyrosine residues on thyroglobulin and the coupling reaction

consists of thiourylenes, anti-thyroid drugs

e. g. propylthiouracil (PTU)
e. g. carbimazole (CBZ)

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17
Q

what are the uses of thionamides?

A

e.g. propothiouricil, carbimazole

  • daily for Graves nodules
  • treatment prior to surgery
  • reduction of symptoms while waiting for radio iodine to act
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18
Q

what are the actions of thioamides?

A
  • inhibits thyroperoxidase and peroxidase transaminase
  • supresses antibody production in Grave’s
  • reduces T4 conversion to T3 in peripheral tissues

remember: tyrosine residues of thyroglobulin are iodinated

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19
Q

biochemical and clinical effect of thionamides/thionureylenes

why does the clinical effect take longer

A

biochemical effect in hours
clinical effect takes weeks

due to large store of thyroxine already present in the thyroid that needs to be removed

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20
Q

why are beta blockers used despite not having effects on thyroxine synthesis?

A

treat symptoms of tachycardia and reduce tremor

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21
Q

unwanted action of thionamides

A
  • agranulocytosis (rare and reversible)

- rashes (common)

22
Q

what thionamide drug is preferentially used

A

carbimazole due to its weaker side effect profile
PTU is potent

however in pregancy, PTU is used over Carbimazole (which crosses the placenta readily)

23
Q

pharmacokinetics of the thionamides

A
  • orally active
  • carbimazole is a prodrug
  • half life of 6-15 hours
  • crosses placenta (secreted in breastmilk)
  • metabolised in the liver and excreted in the urine
24
Q

what is the prodrug carbimazole converted into?

A

converted to methimazole first (administered in the USA)

25
Q

which thianomide drug crosses the placenta more readily

A

carbimazole more than PTU

26
Q

how long is treatment plan with thionamides?

A

18 month plan (stops after that)

review patient frequently for relapse or remission

27
Q

what beta blocker is given

A

propanolol

non selective beta blocker until the other drugs take clinical effect

28
Q

when is KI used?

A

preparation for hypothyroid patient for surgery

also in severe cases e.g. thyroid storm

29
Q

mechanism of action of potassium iodide

A

inhibits iodination of TG

inhibits hydrogen peroxide generation

30
Q

what is the Wolf-Chaikoff effect?

A

presumed reduction in thyroid hormone levels caused by ingestion of a large amount of iodine (KI) which blocks iodine production

symptoms reduce in 1-2 days
size of glands reduce in 10-14 days

31
Q

unwanted reactions of KI

A

allergic reactions

32
Q

pharmacokinetics of KI

A

orally active

Lugol’s solution

33
Q

when is radio iodine used?

how does it target cells?

A

I[131] thyroid cancers and hyperthyroidism

emits beta particles that destroy follicular cells

34
Q

dosage of treatment

A

radioiodine - high dose

technetium 99 pertechnetate- lose dose

35
Q

dosage of radio iodine for Graves and Thyroid cancer

A

graves ~500 MBq

cancer ~3000 MBq

36
Q

radioactive half life of radio iodine

A

8 days

radioactivity negligible after 2 months

37
Q

precautions that need to be taken for those taking radio iodine

A
  • avoid contact with small children for several weeks

- contraindicated in pregnancy and breast feeding

38
Q

what are some investigations for hyperthyroidism?

A
  • blood test for T4, TSH and antibodies

- uptake scan (radioiodine)

39
Q

what does carbimazole do?

A

block synthesis of thyroxine

NB avoid in pregnancy

40
Q

what is used to treat symptoms of hyperthyroidism?

A

beta blockers

41
Q

what occurs in thyroid crises?

A

1) myxoedema coma

2) thyroid storm

42
Q

what occurs in myxoedema coma?

A
  • hypothermia
  • hypotension
  • hypoglycaemia
  • hypoarousal
43
Q

how is myxoedema coma (thyroid crisis) treated?

A

IV liothyronine (synthetic T3)

44
Q

what occurs in thyroid storm?

A
  • hypertension
  • hyperthermia
  • tachycardia and arrhythmia
  • diarrhoea and vomiting
45
Q

how is thyroid storm treated?

A
  • IV beta blockers (for tachycardia)

- Lugoi’s iodine (KI)

46
Q

what effect does Lugol’s iodine work in treating thyroid storm?

A

Wolff-Chaikoffs effect

–> increased iodine consumption decreases thyroxine production

47
Q

what cells do medullary thyroid cancers arise from?

A

parafollicular cells

48
Q

what is a fatal side effect of thionamides?

A

agranulocytosis

49
Q

what is the main issue in Grave’s?

A

autoimmune stimulation

anti-TSH receptor antibodies

50
Q

what symptoms are specific to Graves?

A
  • pretibial myxoedema
  • exophthalmos
  • thyroid acropachy
    (digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.)

LCRS Endo (18 decks)

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