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Internal medicine (small) > Endocrinology (second year) > Flashcards

Endocrinology (second year) Flashcards

1
Q

what are the two endogenous thyroid hormones?

A

T3 - triiodothyronine
T4 - thyroxine

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2
Q

what regulates the synthesis and secretion of thyroid hormone?

A

thyrotropin releasing hormone (TRH)
thyroid stimulating hormone (TSH/thyrotropin)

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3
Q

what component in plasma will influence thyroid hormone synthesis and release?

A

plasma iodide

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4
Q

is there a larger pool of T3 or T4 in blood?

A

T4 (this is converted to T3)

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5
Q

why is T3 not found as abdunantly in blood as T4?

A

T3 is far more active and has a much faster turnover rate, it is also largely found intracellularly

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6
Q

what are the two main effects of endogenous thyroid hormones?

A

stimulation of metabolism
growth and development

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7
Q

how do thyroid hormones effect metabolism?

A

increased metabolism of carbohydrates, fats, protein

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8
Q

how can hyperthyroidism effect the heart?

A

increased heart rate and possible dysrhythmias (atrial fibrillation…)

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9
Q

what effect do thyroid hormones have on the body associated with growth and development?

A

normal skeletal development
maturation of nervous system
promote milk production

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10
Q

how is excess calories (glucose…) made available by feeding stored?

A

glycogen or fat

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11
Q

what is the most important hormone for regulating blood glucose control?

A

insulin

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12
Q

what stimulates insulin production?

A

increased blood glucose

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13
Q

what stimulates glucagon production?

A

decreased blood glucose

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14
Q

what hormones does decreased blood glucose stimulate release of?

A

glucagon, adrenaline, glucocorticoids, growth hormone

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15
Q

where is insulin secreted from?

A

beta cells in the islets of langerhan

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16
Q

where is glucagon secreted from?

A

alpha cells in the islets of langerhan

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17
Q

where is somatostatin secreted from?

A

D cells in the islets of langerhan

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18
Q

what is somatostatin also known as?

A

growth hormone inhibiting hormone

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19
Q

what are the main three locations insulin acts on?

A

liver, fat, muscle

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20
Q

is insulin an anabolic or catabolic hormone?

A

anabolic

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21
Q

what is the overall effect of insulin?

A

conserve fuel by facilitating uptake ad storage of glucose, amino acids and fats (reduces blood glucose)

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22
Q

what processes does insulin inhibit in the liver?

A

glycogenolysis
gluconeogenesis

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23
Q

what process does insulin effect in the muscles?

A

unregulated glucose transporters to allow increased glucose uptake and promote glycogen synthesis

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24
Q

how does insulin effect the brain?

A

the blood brain barrier is not sensitive to insulin so will not have an effect directly on the brain
CSF glucose concentration is directly proportional to blood

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25
Q

what stimulates glucagon secretion?

A

low glucose and fatty acids in plasma

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26
Q

how do amino acids affect glucagon secretion?

A

high amino acids increase the secretion of glucagon

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27
Q

how do sympathetic and parasympathetic activity effect glucagon secretion?

A

both increase the secretion and production of glucagon

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28
Q

what are the main actions of insulin?

A

increase glucose uptake
increase glycogen synthesis
decrease glycogenolysis
decrease gluconeogenesis

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29
Q

what are the main functions of glucagon?

A

increase glycogenolysis
increase gluconeogenesis

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30
Q

what is the major difference in the constituents that make up T3 and T4?

A

T3 has 3 iodines
T4 has 4 iodines

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31
Q

how are thyroid hormones transported in blood?

A

protein bound (not soluble in plasma)
and free

32
Q

what happens to T4 in cells?

A

converted to T3 (active form)

33
Q

what blood tests are available for diagnosing thyroid disease?

A

total T4
free T4
endogenous canine TSH
thyroglobulin autoantibodies

34
Q

what produces endogenous TSH?

A

pituitary gland

35
Q

what is sick euthyroid syndrome?

A

a syndrome by which any disease can suppress T4 (degree of suppression tends to correlate with severity of illness) so total and free T4 tests aren’t very useful

36
Q

why is sick euthyroid syndrome an issue?

A

can alter interpretation of tests (don’t think that because the thyroid hormone is slightly low they have a thyroid issue if there are no other clinical signs)

37
Q

what is the most common endocrine issue?

A

hypothyroidism

38
Q

how can we test for hypothyroidism?

A

serum total and free T4

39
Q

if an animal is showing clinical signs of hypothyroidism and has low T4 what can be done?

A

investigate further - endogenous TSH, thyroglobulin autoantibodies
therapeutic trial

40
Q

how is hypothyroidism treated?

A

replacement therapy - levothyroxine (T4), liothyronine (T3)

41
Q

how is thyroid replacement therapy administer?

A

orally (absorbed by GI tract)

42
Q

what effects will thyroid hormone replacement therapy have?

A

normal growth and development (growth hormone secretion)
increase metabolic rate (heat production)
stimulate cardiovascular system (increase CO and sensitivity to catecholamines)
enhance carbohydrate uptake and lipolysis
promote milk production

43
Q

what are the adverse effects of hormone replacement therapy?

A

signs of hyperthyroidism (given too much)

44
Q

how is hyperthyroidism tested for?

A

serum total T4

45
Q

what should be done if an animal shows signs of hyperthyroidism but total T4 is abnormally high?

A

T3 suppression test

46
Q

how is a T3 suppression test carried out?

A

take basal total T4
give oral T3 for 3 days
if animal has hyperthyroidism they won’t respond in a normal way so their T4 will remain high

47
Q

how should a clinically normal animal respond to the T3 suppression test?

A

the T4 will decrease as they are being supplied with T3

48
Q

how is hyperthyroidism treated?

A

removal of thyroid tissue (surgery/radioactive iodide)
reduce synthesis of thyroid hormone (restrict iodine)

49
Q

what drug blocks synthesis of thyroid hormone?

A

thioureylenes (carbimazole)

50
Q

what is one of the main risks of surgical thyroidectomy?

A

risk of damage to parathyroid hormone (can be problematic if bilateral)

51
Q

how long does it take T3 and T4 for normalise after radioactive iodide treatment?

A

1-2 weeks

52
Q

what is the main risk of radioactive iodide?

A

animals will need to be hospitalised for 1-4 weeks taking care with excreta until radioactivity is gone (also very expensive)

53
Q

what is the main adverse effect of thyroidectomy and radioactive iodide?

A

hypothyroidism

54
Q

what can damage to parathyroid glands during thyroidectomy lead to?

A

hypocalcaemia

55
Q

what cats are suitable candidate for dietary restricted iodine?

A

indoor cats (this is all they can eat)

56
Q

how does carbimazole work?

A

it is metabolised to methimazole which then inhibits T3 and T4 synthesis

57
Q

how is carbimazole administered?

A

orally

58
Q

how is carbimazole metabolised?

A

in the liver (P450 enzyme)

59
Q

what is the adverse effect of carbimazole?

A

hypothyroidism

60
Q

what are the three types of hormones produced by the adrenal gland cortex?

A

glucocorticoids (cortisol)
mineralocorticoids (aldosterone)
sex hormones

61
Q

what blood tests are available for diagnosing disorders of the adrenal cortex?

A

cortisol
aldosterone
ACTH
electrolytes

62
Q

what dynamic tests are available for diagnosing disorders of the adrenal cortex?

A

dexamethasone suppression test
ACTH stimulation test

63
Q

what happens during an ACTH stimulation test?

A

measure basal cortisol level
take blood cortisol 30-60 minutes after synthetic ACTH injection
cortisol should increase in a normal animal

64
Q

what do you need to be careful of when doing ACTH stimulation tests?

A

if animal is taking exogenous glucocorticoids it will interfere with the results

65
Q

what happens during the dexamethasone suppression test?

A

basal blood cortisol measured
take blood cortisol following injection of synthetic glucocorticoid (dexamethasone)
normal animals will get clear suppression of basal cortisol

66
Q

what is hyperadrenocorticism?

A

excess production of cortisol

67
Q

what are the two main causes of hyperadrenocorticism?

A

spontaneous - pituitary-dependant hyperadrenocorticism (PDH), adrenal-dependant hyperadrenocorticism
iatrogenic (medication overise)

68
Q

what are the spontaneous causes of hyperadrenocorticism?

A

pituitary-dependant hyperadrenocorticism (PDH)
adrenal-dependant hyperadrenocorticism

69
Q

how can over-production of hormones from the adrenal cortex be treated?

A

adrenal steroid synthesis inhibitors (trilostane)
mineralocorticoid receptor antagonists

70
Q

what type of inhibitor is trilostane?

A

competitive

71
Q

what are the adverse effects of trilostane?

A

hypoadrenocorticism
electrolyte abnormalities
inhibits progesterone synthesis (don’t use in pregnancy)

72
Q

what drug is a mineralocorticoid receptor antagonist but normally used as a diuretic?

A

spironolactone

73
Q

what is hyperadrenocorticism also known as?

A

cushings

74
Q

what is hypoadrneocorticism also known as?

A

addisons

75
Q

how can hypoadrenocorticism (Addisons) be cause iatrogenically?

A

through sudden withdrawal of prolonged high doses of glucocorticoids

76
Q

what drug is used to treat Addisons as a mineralocorticoid receptor agonist?

A

desoxycortone pivalate
(can use aldosterone but has very short half life)

77
Q
A

Internal medicine (small) (33 decks)

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