Y2 ENDOCRINE THYROID CONDITIONS AND TREATMENT Flashcards

1
Q

management of medullary thyroid cancer in MEN2?

A

prophylactic thyroidectomy.

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2
Q
  • raised serum calcium
  • raised serum PTH or inappropriately normal
  • increased urine calcium excretion.
A

primary hyperparathyroidism

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3
Q

Hypercalcaemia of malignancy due to?

A
  • metastatic bone destruction
  • PTH related protein from solid tumours
  • osteoclast activating factors
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4
Q

management of primary hyperparathyroidism?

A

SURGERY OR NOTHING

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5
Q

what are the indications for parathyroidectomy?

A
  • end organ damage (bone disease, gastric ulcers, renal stones, osteoporosis).
  • v. high calcium
  • if under 50
  • if eGFR <60ml/min
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6
Q

primary overactivity of parathyroid e.g. adenoma.

A

primary hyperparathyroidism

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7
Q

physiological response to low calcium.

A

secondary hyperparathyroidism

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8
Q

parathyroid becomes autonomous after years of secondary disease.

A

tertiary hyperparathyroidism

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9
Q

what structures are at risk during thyroid surgery?

A
  • recurrent laryngeal nerves

- parathyroid glands

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10
Q

what causes a midline neck mass in adults?

A
  • enlarged thyroid gland
  • enlarged lymph nodes
    Rare outwith childhood:
  • thyroglossal cyst
  • cystic hygroma
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11
Q

how do you differentiate between diffuse and focal thyroid pathology?

A
  • radioisotope studies

- ultrasound

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12
Q

when do you ultrasound the thyroid?

A
  • euthyroid patients with goitre/palpable nodules.

- hyperthyroid with focal masses/ radioisotope uptake

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13
Q

why use thyroid scintigraphy?

A

to assess pattern and quantity of tracer uptake.

  • homogenous increased uptake = graves.
  • homogenous reduced uptake = thyroiditis.
  • focal uptake = multinodular goitre with dominant nodule
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14
Q

homogenous increased uptake in thyroid scintigraphy?

A

graves

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15
Q

homogenous reduced uptake in thyroid scintigraphy?

A

thyroiditis

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16
Q

focal uptake in thyroid scintigraphy?

A

multinodular goitre with dominant nodule

17
Q

lytic lesion?

A

bone destruction

18
Q

sclerotic lesion?

A

bone formation

19
Q

diffuse brittle bones?

A

osteoporosis

20
Q

diffuse soft bones?

A
  • rickets/osteomalacia

- pagets disease

21
Q

what may cause hypoparathyroidism?

A
  • congenital absence (DiGeorge syndrome)
  • destruction (surgery, radiotherapy, malignancy).
  • autommune
  • hypomagnesaemia
  • idiopathic
22
Q

management of hypoparathyroidism?

A
  • calcium supplement >1-2g/day.

vitamin D:

  • tablets i.e. 1-alpha-calcidol 0.5-1mcg/day
  • depot injection of cholecalciferol 300,000 units 6 monthly.
23
Q

calcium release from cells is dependent on?

A

magnesium

24
Q

in magnesium deficiency, intracellular calcium is?

A

high

25
Q

in magnesium deficiency, what happens to PTH release?

A

it is inhibited

26
Q

management of hypomagnasaemia?

A

magnesium + calcium if low.

27
Q

what happens to skeletal and muscle receptors of PTH in hypomagnasaemia?

A

they become less sensitive to PTH

28
Q

causes of hypomagnasaemia?

A
  • alcohol
  • drugs e.g. thiazides and PPI
  • GI illness, pancreatitis, malabsorption.
29
Q

what biochemical abnormalities are seen in pseudohypoparathyroidism?

A
  • low calcium

- elevated PTH

30
Q

what biochemical abnormalities are seen in pseudopseudohypoparathyroidism?

A
  • normal calcium

- high PTH

31
Q

what may occur as a result of chronic renal disease?

A
  • vit. D deficiency

- secondary hyperparathyroidism.

32
Q

management of vit. D deficiency/secondary hyperparathyroidism due to chronic renal disease?

A
  • phosphate binders
  • titrate treatments to PTH levels
  • check 1-25, OH vit. D