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Year 4 > Endocrinology 1 > Flashcards

Endocrinology 1 Flashcards

1
Q

nervous vs endocrine system?

A 
nervous = fast on and fast off
endocrine = slow on and slow off
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2
Q

main endocrine organs?

A 
pituitary
thyroid
pancreas
adrenals
gonads
parathyroids
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3
Q

what does anterior pituitary produce?

A 
FLAT PIG
FSH
LH
ACTH
TSH
prolactin
intermediate - MSH
Growth hormone
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4
Q

what does posterior pituitary make?

A

oxytocin

ADH

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5
Q

what does pancreas make?

A

insulin (beta cells)

glucagon (alpha cells)

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6
Q

what do adrenals make?

A

mineralocorticoids - aldosterone
glucocorticoids - cortisol
adrenal androgens - DHEA
adrenaline and noradrenaline

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7
Q

where are most androgens made?

A

gonads

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8
Q

steps in establishing endocrine disorder?

A

look for phenotype first
then check biochemistry
if biochemical abnormality confirmed then do imaging to check for anatomical problem (eg adenoma in pituitary)
then look at treatment

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9
Q

basics of testing hormone levels?

A

if worried about too much hormone then try and suppress it

if worries about too little hormone then try to stimulate it

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10
Q

things to be aware of when testing hormone levels?

A

some hormones arent secreted at constant level (eg some have diurinal variation or growth hormone which is released in bursts)

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11
Q

general rule for endocrine imaging?

A

CT best for abdominal (eg adrenals)

MRI best for pituitary

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12
Q

main functions of thyroid?

A

produces T3, T4 and calcitonin

regulates metabolism

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13
Q

job of parathyroid?

A

calcium regulation

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14
Q

job of adrenals?

A

fight or flight

emergency control centre

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15
Q

layers of adrenals?

A

outer cortex - aldosterone, cortisol and androgens

inner medulla - adrenaline and noradrenaline

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16
Q

zones of adrenals?

A

zona glomerulosa
zona faciculata
zona reticularis

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17
Q

what is MSH?

A

melanocyte stimulating hormone

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18
Q

most common endocrinopathy?

A

diabetes then thyroid

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19
Q

are thyroid hormones stable?

A

yes

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20
Q

features of hyperthyroidism?

A 
tachycardia
weight loss
sweating/heat intolerance
loose stools
exophthalmos
irregular periods or amenorrhoea
fine tremor 
anxiety
trouble sleeping
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21
Q

thyroid biochemistry?

A

production is 80% T4 and 20% T3

T3 is the active hormone (T4 becomes deiodinated)

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22
Q

primary hyperthyroid biochemistry?

A

low TSH and high T4

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23
Q

secondary hyperthyroid biochemistry? (problem in pituitary or rarely in hypothalamus)

A

high TSH and high T4

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24
Q

causes of primary hyperthyroid?

A

graves disease (autoimmune)
toxic multinodular goitre
solitary toxic adenoma (hot nodule)
can sometimes get a thyroiditis where inflammation can initially cause increased release of hormones before becoming hypothyroid

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25
Q

causes of secondary hyperthyroid?

A

TSH secreting pituitary tumour
exogenous T3 or T4 (factitious or iatrogenic hyperthyroidism)
ectopic thyroid tissue

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26
Q

what is graves disease?

A 
autoimmune hyperthyroidism (most common cause of hyperthyroid)
thyroid receptor antibodies (Trab) attach onto TSH receptors, stimulating uptake of iodine into thyroid and production of T4 and T3
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27
Q

other symptoms of graves?

A 
eye disease (exopthalmos)
thyroid acropachy (clubbing)
pre-tybial myxoedema
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28
Q

management of exopthalmos in graves disease?

A

can be an emergency if pressure increases

steroids given

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29
Q

diagnosis of hyperthyroid?

A

thyroid function tests
can measure Trab antibodies (+ve = graves, -ve = do US to look for other cause)
thyroid uptake scans then done to check if single/multi and functionality (diffuse uptake = graves)

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30
Q

features of graves disease on investigation?

A 
low TSH high T4
\+ve Trab antibodies
smooth goitre
uniform uptake scan
uniform gland on US and palpation
can have bruits (indicates increased blood supply)
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31
Q

what is multinodular goitre?

A

lots of areas of normal looking thyroid tissue which has gotten out of control and no longer listening to pituitary

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32
Q

what can cause thyroiditis?

A

autoimmune
post-partum
amiodarone

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33
Q

pattern of thyroiditis?

A

inflammation causes all thyroid hormone reserves to be chucked out of the thyroid
so initially hyperthyroid then hypothyroid

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34
Q

medical management of hyperthyroidism?

A

carbimazole (mainstay)
propothiouracil (PTU)
beta blockers can be used to help symptoms while waiting on carbimazole/PTU to work (non-selective ones such as propanalol)
radioactive iodine (taken up into thyroid and radiation obliterates the thyroid)

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35
Q

side effects of carbimazole?

A

agranulocytosis (loss of neutrophils)

jaundice (more common in PTU)

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36
Q

important monitoring with carbimazole?

A

must get immediate FBC and stop drug if they get a sore throat

37
Q

side effects of PTU?

A

jaundice

autoimmune hepatitis

38
Q

when is PTU used first line?

A

pregnancy (esp first trimester)

39
Q

treatment success in graves disease?

A

50% chance of cure in 18 months with treatment

40
Q

are steroids given in hyperthyroidism?

A

no

only if concerned about eyes

41
Q

risks of radioactive iodine?

A

often need more than one dose
can cause hypothyroid
radiation damage which can spread to other people (ie need to isolate from family, work etc)

42
Q

surgical management of hyperthyroidism?

A

lobectomy

thyroidectomy

43
Q

risks of thyroid surgery?

A

damage to recurrent laryngeal nerve

accidental removal/damage of parathyroid causing hypocalcaemia etc

44
Q

what is a thyroid storm?

A

extreme hyperthyroid with high mortality

45
Q

features of thyroid storm?

A 
cardio (v tachycardiac, arrhythmias, heart failure)
fluid loss in diarrhoea, sweat etc
v. aggitated
seizures and coma
cant regulate body temp
46
Q

management of thyroid storm?

A

carbimazole/PTU via NG tube
give lots of fluid (be aware of heart failure)
beta blockers (maybe IV)
high dose iodine
can give lithium
may need to be paralysed and ventilated to cool down the body

47
Q

where is hypothyroid seen most often?

A

GP

usually not a primary presenting problem in hospital

48
Q

hypothyroid phenotype?

A 
weight gain
cold intolerance 
constipation
tired
menorrhagia 
bradycardia 
can have fluid excess
49
Q

primary hypothyroid biochemistry?

A

high TSH

low T4

50
Q

secondary hypothyroid biochem?

A

TSH and T4 both low

51
Q

how is hypothyroid managed?

A

levothyroxine (titrate until TSH and T3/T4 in normal range)

T3/T4 combination can be given in rare cases

52
Q

causes of primary hypothyroid?

A 
idiopathic
hashimotos (autoimmune)
radiation (including radioactive iodine)
hyperthyroid treatment
surgery
fibrosis of thyroid
iodine deficiency
53
Q

what causes hashimotos?

A

antibodies against thyroid peroxidase enzymes
peroxidase part of structure of thyroid where hormone is made so hashimotos causes destruction of hormone producing tissues

54
Q

how does hashimotos affect thyroid hormone levels?

A

initially hyperthyroid as all the T3/T4 are thrown out of the thyroid then ultimately become hypothyroid

55
Q

causes of secondary hypothyroid?

A

pituitary or hypothalamus neoplasm
congenital hypopituitarism
sheehans syndrome (lack of blood supply to pituitary often after post partum haemorrhage)

56
Q

other causes of hypothyroid?

A

amiodarone
lithium
infiltrative diseases (sarcoidosis, amyloidosis, scleroderma, haemochromatosis)

57
Q

extreme form of hypothyroid?

A

myxoedema

58
Q

features of myxoedema?

A

very cold
v bradycardic (can result in heart failure which causes oedema)
loss of outer 1/3 of eyebrows
thin hair
menorrhagia
can have carpal tunnel as a result of fluid retention compressing nerve
hypothermia

59
Q

lab findings in myxoedema?

A

hyponatraemia (low thyroxine causes SIADH)
pericardial effusion
hypoglycaemia
long QT

60
Q

management of myxoedema?

A

support airway
get them warm
give steroids (hydrocortisone)
give lots of thyroxine

61
Q

what must you be aware of when giving thyroxine in myxoedema?

A

dont give to much in heart failure

suddenly drives heart rate and basal metabolic rate which can cause a decompensation

62
Q

why are steroids given in myxoedema?

A

reduces any inflammation
often autoimmune so helps with that
people can have lack of steroids from co-existent addisons disease

63
Q

where are the parathyroid glands found?

A

behind thyroid

usually 4 of them

64
Q

how is vitamin D formed?

A

sunlight hits the skin and converts cholesterol into vitamin D3 (main source)
also have dietary sources

65
Q

dietary sources of vit D?

A

milk
oily fish
cheese
tuna

66
Q

what happens to vit D3?

A

goes to the liver where its activated (hyroxylated) to 25 OH Vit D

67
Q

what happens to 25 OH Vit D?

A

travels to the kidney where another OH is added at 1 position to become 1,25 OH Vit D

68
Q

why does kidney disease cause problems with calcium metabolism?

A

kidneys cant hydroxylate 25 OH vit D to 1,25 OH vit D meaning the Vit D is much less effective

69
Q

normal calcium range?

A

2.2-2.6 mmol/L

70
Q

hypercalcaemia symptoms?

A 
confusion
lethargy
depression
bones (osteoporosis)
stones (renal stones)
moans (constipation)
groans (psychiatric)
71
Q

what other hormone is important for calcium metabolism?

A

PTH

produced more when parathyroids sense low calcium

72
Q

what does PTH do when calcium is low?

A

stimulates 1 alpha hydroxylase enzyme to hydroxylate vit D to 1,25 OH vit D
increases calcium reabsorption in kidney
increases phosphate secretion through kidney
acts on osteoclasts to resorb bone causing bone thinning

73
Q

main action of 1,25 OH vit D?

A

acts in the gut to increase calcium and phosphate resorption

74
Q

role of magnesium in calcium metabolism?

A

parathyroid hormone cant work effectively without magnesium

magnesium also needed to release PTH from the gland

75
Q

primary hyperthyroidism?

A

idiopathic inappropriate secretion of PTH
increased PTH and calcium
low phosphate

76
Q

secondary hyperparathyroidism?

A

hypersecretion of PTH secondary to low calcium (can be due to vit D deficiency or kidney disease etc)
high PTH
low calcium and phosphate
(high PTH is appropriate response to low calcium from some other cause so system working correctly)

77
Q

tertiary hyperparathyroidism?

A

secondary hyperparathyroid has gone on so long that the gland has got out of control and formed adenomas which arent under any regulation
can cause extremely high PTH and calcium and very low phosphate
more common in CKD

78
Q

phenotype of hyperparathyroid?

A 
features of hypercalaemia (bones, groans, stones, moans)
polyuria and polydipsia 
osteoporosis
lethargy
confusion
79
Q

how do you prove hyperparathyroidism?

A

calcium and PTH are stable so no point trying to suppress

phenotype > biochemistry > imaging

80
Q

imaging in primary hyperparathyroidism?

A

sestimibi scan
techenium 99 labelled sestimibi (similar to PTH precursors) is taken up into offending parathyroid gland and lets surgeon know which one is causing problem and needs removal

81
Q

management of hyperparathyroidism?

A

laparoscopic surgery

bisphosphonates can help with bone symptoms

82
Q

key test to do in hypercalcaemia?

A

PTH
high PTH = primary hyperparathyroid
low PTH = PTH appropriately suppressed due to high calcium from another cause such as malignancy

83
Q

which MEN can cause hypercalcaemia?

A

MEN 1 (parathyroid adenoma)

84
Q

what is familial hypocalciuric hypercalcaemia?

A

body thermostat for calcium set at a higher level so body keep calcium high
high calcium is normal and harmless for these patients

85
Q

how can malignancy cause hypercalcaemia?

A

usually metastatic or primary which causes release of parathyroid hormone related peptide

86
Q

types of primary cancer which can cause hypercalcaemia?

A

breast
lung
bone
myeloma

87
Q

how can granulomatous diseases such as sarcoid and TB cause high calcium?

A

these granulomas can hydroxylate Vit D as well as the kidneys so theres extra active vit D causing more calcium absorption

88
Q

what medications can cause high calcium?

A

lithium
thiazides
vit D

Year 4 (83 decks)

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