hypERthyroid Flashcards

1
Q

primary vs secondary hyperthyroidism

A

primary - due to thyroid pathology

seocndary - due to pathology in hypothalamus or pituitary - producing too much TSH

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2
Q

Graves disease

A

autoimmune thyroid disease
- body produces IgG antibodies to the TSH receptor

women 30-50yrs

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3
Q

commonest cause of thyrotoxicosis

A

Graves

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4
Q

Graves presentation

A

eye signs
- exophthalmos
- ophthalmoplegia

pretibial myxoedema

thyroid acropachy, triad;
1. digital clubbing
2. soft tissue swelling of hands+feet
3. periosteal new bone formation

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5
Q

antibodies present in Graves

A

TSH receptor stimulating antibodies (90%)

anti-thyroid peroxidase antibodies (10%)

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6
Q

Graves investigations

A

autoantibodies
thyroid scintigraphy
- diffuse
- homogenous
- increased uptake of radioactive iodine

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7
Q

management of Graves

A

1st = anti-thyroid drugs - carbimazole (give if sx not controlled with propran)

propranolol = symptoms control

refer to 2nd care

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8
Q

carbimazole complications

A

! Agranulocytosis !

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9
Q

treatment with anti-thyroid drugs (ATD) such as carbimazole

A

started at 40mg, reduced gradually to maintain euthyroidism
- continued for 12-18months

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10
Q

when is radioiodine treatment used? what are the contraindications

A

in patients who relapse following ATD therapy or resistant to ATD tx

contraindications
- pregnancy - avoid 4-6mths following
- age <16
- thyroid eye disease - may worsen

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11
Q

amiodarone effect on thyroid

A

can cause both hypothyroidism + thyrotoxocosis

due to high iodine content

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12
Q

subclinical hyperthyroidism

A

normal serum free thyroxine
with LOW TSH

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13
Q

causes of subclinical hyperthyroidism

A
  • multinodular goitre, esp in elderly females
  • excessive thyroxine may give similar biochem picture
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14
Q

complications of unrecognised subclinical hyperthyroidism

A

effect on -
- cardiovas - atrial fibrillation
- bone metabolism - osteoporosis

increase likelihood of dementia

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15
Q

management of subclinical hyperthyroidism

A

often go back to normal - TSH levels must be persitently low to intervene

trial of low-dose antithyroid agent for 6 months to induce remission

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16
Q

causes of thyrotoxicosis

A
  • graves (50-60%)
  • acute phase of de Querv thyroiditis, post partum or hashimotos
  • amiodarone therapy
  • contrast (iodinated contrast)
    –> tend to occur in elderlywith pre-exist thyroid probs
17
Q

TSH + T3/4 in thyrotoxicosis

A

TSH down
T4/3 up

18
Q

features of thyrotoxicosis

A

weight loss
heat intolerance
manic, restlessness
palpitations
sweating
tremor
pretibial myxoedema

19
Q

pretibial myxoedema

A

erythematous
oedematous lesions above lateral malleoli

20
Q

gynae changes in hyper vs hypo-thyroidism

A

hyper = oligomenorrhoea

hypo = menorrhagia

21
Q

thyroid storm

A

rare but life threatening cx of thyrotoxicosis
- seen in patients with well established thyrotoxicosis

NOT see in iatrogenic thyroxine excess

22
Q

thyroid storm precipitating events

A

thyroid/non-thyroid surgery
trauma
infection

acute iodine load - CT contrast

23
Q

thyroid storm presentation

A

fever >38.5
tachycardia
confusion, agitation
N+V
hypertension
heart failure
abnormal LFTs - jaundice

24
Q

mangement of thyroid storm

A

beta-blockers - IV propranolol
ATD - methimazole or propylthiouracil

decamethasone IV -> blocks conversion of T4-T3

25
Q

toxic multinodular goitre Ix + Mx

A

nuclear scintigraphy = patchy uptake

Mx = radioiodine therapy

26
Q

toxic multinodular goitre Ix

A

thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism