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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
what stimulates glucagon secretion?
low glucose and fatty acids in plasma
26
how do amino acids affect glucagon secretion?
high amino acids increase the secretion of glucagon
27
how do sympathetic and parasympathetic activity effect glucagon secretion?
both increase the secretion and production of glucagon
28
what are the main actions of insulin?
increase glucose uptake increase glycogen synthesis decrease glycogenolysis decrease gluconeogenesis
29
what are the main functions of glucagon?
increase glycogenolysis increase gluconeogenesis
30
what is the major difference in the constituents that make up T3 and T4?
T3 has 3 iodines T4 has 4 iodines
31
how are thyroid hormones transported in blood?
protein bound (not soluble in plasma) and free
32
what happens to T4 in cells?
converted to T3 (active form)
33
what blood tests are available for diagnosing thyroid disease?
total T4 free T4 endogenous canine TSH thyroglobulin autoantibodies
34
what produces endogenous TSH?
pituitary gland
35
what is sick euthyroid syndrome?
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
why is sick euthyroid syndrome an issue?
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
what is the most common endocrine issue?
hypothyroidism
38
how can we test for hypothyroidism?
serum total and free T4
39
if an animal is showing clinical signs of hypothyroidism and has low T4 what can be done?
investigate further - endogenous TSH, thyroglobulin autoantibodies therapeutic trial
40
how is hypothyroidism treated?
replacement therapy - levothyroxine (T4), liothyronine (T3)
41
how is thyroid replacement therapy administer?
orally (absorbed by GI tract)
42
what effects will thyroid hormone replacement therapy have?
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
what are the adverse effects of hormone replacement therapy?
signs of hyperthyroidism (given too much)
44
how is hyperthyroidism tested for?
serum total T4
45
what should be done if an animal shows signs of hyperthyroidism but total T4 is abnormally high?
T3 suppression test
46
how is a T3 suppression test carried out?
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
how should a clinically normal animal respond to the T3 suppression test?
the T4 will decrease as they are being supplied with T3
48
how is hyperthyroidism treated?
removal of thyroid tissue (surgery/radioactive iodide) reduce synthesis of thyroid hormone (restrict iodine)
49
what drug blocks synthesis of thyroid hormone?
thioureylenes (carbimazole)
50
what is one of the main risks of surgical thyroidectomy?
risk of damage to parathyroid hormone (can be problematic if bilateral)
51
how long does it take T3 and T4 for normalise after radioactive iodide treatment?
1-2 weeks
52
what is the main risk of radioactive iodide?
animals will need to be hospitalised for 1-4 weeks taking care with excreta until radioactivity is gone (also very expensive)
53
what is the main adverse effect of thyroidectomy and radioactive iodide?
hypothyroidism
54
what can damage to parathyroid glands during thyroidectomy lead to?
hypocalcaemia
55
what cats are suitable candidate for dietary restricted iodine?
indoor cats (this is all they can eat)
56
how does carbimazole work?
it is metabolised to methimazole which then inhibits T3 and T4 synthesis
57
how is carbimazole administered?
orally
58
how is carbimazole metabolised?
in the liver (P450 enzyme)
59
what is the adverse effect of carbimazole?
hypothyroidism
60
what are the three types of hormones produced by the adrenal gland cortex?
glucocorticoids (cortisol) mineralocorticoids (aldosterone) sex hormones
61
what blood tests are available for diagnosing disorders of the adrenal cortex?
cortisol aldosterone ACTH electrolytes
62
what dynamic tests are available for diagnosing disorders of the adrenal cortex?
dexamethasone suppression test ACTH stimulation test
63
what happens during an ACTH stimulation test?
measure basal cortisol level take blood cortisol 30-60 minutes after synthetic ACTH injection cortisol should increase in a normal animal
64
what do you need to be careful of when doing ACTH stimulation tests?
if animal is taking exogenous glucocorticoids it will interfere with the results
65
what happens during the dexamethasone suppression test?
basal blood cortisol measured take blood cortisol following injection of synthetic glucocorticoid (dexamethasone) normal animals will get clear suppression of basal cortisol
66
what is hyperadrenocorticism?
excess production of cortisol
67
what are the two main causes of hyperadrenocorticism?
spontaneous - pituitary-dependant hyperadrenocorticism (PDH), adrenal-dependant hyperadrenocorticism iatrogenic (medication overise)
68
what are the spontaneous causes of hyperadrenocorticism?
pituitary-dependant hyperadrenocorticism (PDH) adrenal-dependant hyperadrenocorticism
69
how can over-production of hormones from the adrenal cortex be treated?
adrenal steroid synthesis inhibitors (trilostane) mineralocorticoid receptor antagonists
70
what type of inhibitor is trilostane?
competitive
71
what are the adverse effects of trilostane?
hypoadrenocorticism electrolyte abnormalities inhibits progesterone synthesis (don't use in pregnancy)
72
what drug is a mineralocorticoid receptor antagonist but normally used as a diuretic?
spironolactone
73
what is hyperadrenocorticism also known as?
cushings
74
what is hypoadrneocorticism also known as?
addisons
75
how can hypoadrenocorticism (Addisons) be cause iatrogenically?
through sudden withdrawal of prolonged high doses of glucocorticoids
76
what drug is used to treat Addisons as a mineralocorticoid receptor agonist?
desoxycortone pivalate (can use aldosterone but has very short half life)
77

Internal medicine (small) (33 decks)

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