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CP > investigation of the endocrine > Flashcards

investigation of the endocrine Flashcards

1
Q

what are hormones?

A

they are messenger molecules that are secreted by endocrine glands

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2
Q

what do hormones do?

A

they circulate and influence other tissues by producing short and long term changes in various cells

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3
Q

which cells do hormones affect?

A

they can only influence cells that have specific target receptors for that particular hormone

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4
Q

what are the three types of hormone and examples of them?

A

peptide hormones, steroid hormones and tyrosine based hormones
peptide - TSH, ACTH and PTH
steroid - testosterone, cortisol and oestradiol
tyrosine based - thyroxine T4 and triiodothyronine T3

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5
Q

how do hormones act?

A

through intercellular signalling
autocrine - releases the molecules and then they act on a receptor on its own cell membrane
paracrine - released directly to the other cell receptors
endocrine - released directly into the bloodstream to distant target cells

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6
Q

how do steroid hormones elicit a response?

A

there are three ways that the steroid hormones can interact with cells
receptor mediated endocytosis
the classical model
signalling through cell surface receptors

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7
Q

what is receptor mediated endocytosis with regards to steroid hormones?

A

when the steroid hormone, bound to the plasma carrier protein is brought into the cell through the cell surface receptor and the complex is broken down in the lysosome. The free hormone then diffuses to the location in cell and exerts action at the genomic or metabolic level

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8
Q

what is the classical model with regards to steroid hormones?

A

the steroid hormones dissociates from the plasma carrier protein and diffuses across the cell membrane. It then binds to an intracellular receptor and will alter gene transcription

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9
Q

what is signalling through cell surface receptors with regards to steroid hormones?

A

the free steroid hormone alters intracellular signalling by binding to the cell surface receptors. The steroid hormone will exert these effects directly or by blocking the actions of peptide hormones

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10
Q

what locations in the body secrete hormones?

A

in the brain there is the pineal gland, the pituitary gland and the hypothalamus. Then the thyroid and parathyroid glands and the thymus. There is also the hand, stomach, duodenum and jejunum and then the kidneys and adrenals. The pancreas, ovary, testes and placenta also secrete

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11
Q

how does the hypothalamus feedback?

A

it has positive feedback to the anterior pituitary and then this has positive feedback to the endocrine organ. The endocrine organ will in turn then have negative feedback on the pituitary which negatively feedsback to the hypothalamus

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12
Q

what does the hypothalamus secrete that feeds back to the a) gonads, b) thyroid, c) breasts, d) adrenal cortex and e) many tissues?

A

the hypothalamus will a) release GnRH which stimulates production of LH and FSH from the pituitary anteriorly and then results in the release of sex hormones from the gonads.

b) TRH stimulates TSH from the ant pituitary to produce thyroxine from the thyroid
c) PRH stimulates prolactin which acts on the breast, and inhibited by dopamine
d) CRH stimulates ACTH which results in cortisol release from adrenal cortex
e) GHRG stimulates GH from ant pituitary and somatostatin inhibits GH from anterior pituitary

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13
Q

what are the causes of increased plasma TBG?

A

genetic, pregnancy or oestrogens

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14
Q

what are the causes of decreased plasma TBG?

A

genetic, acromegaly, malnutrition, protein losing states, malabsorption, cushings, androgens, high dose corticosteroids, severe illness

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15
Q

what is TBG?

A

thyroxine binding globulin

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16
Q

what factors affect TFT interpretation?

A

only the free unbound forms are physiologically active therefore if the level of TBG changes the level of free hormones changes so the measurement of total hormones levels can be misleading

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17
Q

what is the case of TSH in secondary hypothyroidism?

A

in around 84% of cases the TSH is normal with a low fT4, but in around 8% of cases TSH is low (<0.2mU/l) and in around 8% of cases it is high (>3.5mU/L but <10mU/L)

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18
Q

what is the sign of pituitary failure?

A

when TSH and thyroxine are decreased

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19
Q

what is the sign of feedback failure of pituitary gland overproduction?

A

TSH and thyroxine increase

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20
Q

what is the sign of thyroid gland overproduction?

A

when thyroxine increases but TSH decreases

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21
Q

what is the sign of unresponsive thyroid?

A

when there is an increase in TSH but a reduction in Thyroxine

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22
Q

if you are testing TSH, because it is low, what is used and what are the interpretations of results?

A

use free T4 as a marker
if T4 is low then could be central hypothyroidism or severe illness
if T4 is normal then there is T3 toxicosis or subclinical hyperthyroidism
if T4 is elevated then there is hyperthyroidism

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23
Q

why would you not continue to do TSH testing?

A

when the TSH is normal

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24
Q

if TSH is elevated and free T4 is used, what are the interpretations of the results?

A

if the free T4 is low then there is hypothyroidism
if the T4 is normal then there is subclinical hypothyroidism
if there is elevated T4 then there is TSH secreting tumour

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25
Q

why is thyroid function tests only used when thyroid dysfunction is suspected?

A

there is poor predictive value of the thyroid function tests in ill patients as patients suffering from non thyroidal illness may show abnormalities in the thyroid function tests despite being euthryoidic

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26
Q

what changes are there in TSH in illness?

A

TSH levels may be supressed in acute phases of illness
they may transiently rise into the hypothyroidic range in the recovery phase following an illness
illness can also change the level of or alter the ability of TBG to bind to T3 and T4 and therefore there will be differing levels of these

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27
Q

what is the course of TSH throughout illness?

A

when you are well the TSH, rT3 FT4, TT4 and TT3 are within the normal range. However, as illness increases, TSH initially drops with TT3 and TT4 and rT3 and FT4 rise (rT3 massivley). As recovery progressesrT3 peaks and then drops, FT4 drops back down, TSH rises above normal level, and TT4 and TT3 peak and then rise back up to normal. TSH then drops and all return to normal when you are well again. T3 is normally low and then peaks very high at mortality, then drops low again

28
Q

how often should TFTs be repeated in a healthy eperson?

A

every 3 years

29
Q

how often should TFTs be repeated in hyperthyroidism?

A

such as in monitoring graves disease - after 1-2 months after radioactive iodine, if they are still thyrotoxic then every 4-6 weeks and after a thryoidectomy then every 6-8 weeks with levothyroxine

30
Q

how often should TFTs be monitored in hypothyroidism?

A

should not be taken before 2 months after treatment as this is the minimal time it will take for levels to return to normal, but patients stabilised on long term treatment should be checked annually. Also an annual fT4 should be checked in secondary hypo with thyroxine therapy

31
Q

what immunoassays are used in the measurement of thyroidism?

A

sometimes polyclonal ABs and radioisotope labelling, but mainly monoclonal ABs due to H&S reasons - mainly enzymes

32
Q

what are the reasons for widely using monoclonal ABs?

A

they are specific due to the enzyme specificity, they are sensitive as can measure picomolar concentrations and they are amenable to automation

33
Q

what are the main types of immunoassay used in thyroidism?

A

immunometric assays and competitive immunoassays

34
Q

what is the difference in results of the tracer binding in competitive and non competitive assays?

A

in non competitive it is a linear graph - as concentration increases so does tracer binding however in competitive as the concentration of standard increases the tracer binding decreases

35
Q

what sort of interference can there be in assays?

A

there can be a crosslinking antibody - this will cause positive interference, and there can be a blocking antibody which will cause negative interference

36
Q

what are the types of adrenal medullary tumours?

A

there are two types - these are phaeochromocytomas in adults and neuroblastomas in children

37
Q

what is a phaeochromocytoma?

A

it is a tumour of the neuroendocrine chromaffin cells - the majority are in the adrenal medulla however 10% are malignant, 10% are extra adrenal neuroendocrine cells and 5% are bilateral especially as part of MEN 2a or b syndrome

38
Q

what are the clinical features of phaeochromocytomas?

A

these are due to the excessive and episodic release of catecholaminesresulting in paroxysmal features such as headaches, hypertension, panic attacks, sweating, pallor, abdo pain or nothing

39
Q

what is the diagnosis of phaeochromocytoma?

A

it is often difficult - there are false positives and negatives commonly - use plasmametanephrines or 24 hour urine fractionated metanephrines or urinary VMA

40
Q

what are the characteristics of plasmametanephrines?

A

they are unstable so collect on ice, they are not available in many labs and they have a sensitivity of 99% and specificity of 89%

41
Q

what are the characteristics of urine fractionated metanephrines?

A

they have the usual issues of 24 hour collection, sensitivity of 96-100% and a specificity of 94-97% and you have to prepare the patient

42
Q

what needs to be considered when diagnosing phaeochromocytoma?

A

ideally need to stop antihypertensives, certain drugs will cause biological or analytical interference with HPLC measurement

43
Q

what should be considered when using urinary VMA?

A

the patient needs to be on a vanilla free diet

44
Q

what are the follow up tests for phaeochromocytoma?

A 
clonidine supression test 
plasma chromogranin A
MRI or CT of adrenals 
MIBG scan 
genetic counselling and screening for MEN mutations in younger patients or those with a family history
45
Q

what are clonidine supression tests useful for?

A

in those patients with suspected phaemochromocytoma and borderline changes in catecholamines or metanephrines

46
Q

what are the characteristics of plasma chromogranin A?

A

there is a sensitivity of 83% and specificity of 96%

47
Q

what are MBGIs for?

A

for extra adrenal phaeochromocytomas or metastases

48
Q

what is whipples triad?

A

it is for hypoglycaemia
it consists of signs and symptoms of hypoglycaemia
low plasma glucose level of less than 53mg/dL in normal (3mmol) and <63mg/dL in diabetics (3.5mmol)
and the resolution of symptoms once glucose level rises again

49
Q

what are the autonomic signs and symptoms of hypoglycaemia?

A

anxiety, hunger, pallor, sweating, tachycardia, widened pulse pressure, parasthesias, tremulousness, palpitations

50
Q

what are the neuroglycopenic symptoms and signs of hypoglycaemia?

A

cognitive dysfunction, blurred vision, behavioural change, dizziness, weakness and fatigue, headache and confusion
cortical blindness, hy[hypothermia, seizures and coma

51
Q

what are the insulin mediated endogenous causes differential diagnosis of hypoglycaemia?

A

insulinoma, nesidoblastosis, NIPHS, insulin antibodies and reactive (alimentary hypoglycaemia, reactive hypoglycamia associated with T2 diabetes and idiopathic)

52
Q

what are the non insulin mediated endogenous causes differential diagnosis of hypoglycaemia?

A

sepsis, critical organ failure, insulin receptor antibodies, non islet cell tumour or hormone deficiency

53
Q

what are the organs that can fail that is on the differential diagnosis for hypoglycaemia?

A

hepatic disease, cardiac and renal failure

54
Q

what are the therapeutics exogenous causes differential diagnosis of hypoglycaemia?

A

there can be direct effect from drugs or can be interactions with insulin or sulfonylureas
direct - insulin, sulfonylureas, quinine, disopyramide, adrenoreceptor agonists, pentamidine and other
interactions - biguanines, adrenoreceptor blockers, PPAR agonists and ACE inhibitors

55
Q

what other exogenous causes should be on the differential diagnosis for hypoglycaemia?

A

fastidious - felonious

alcohol - toxins

56
Q

what are the features of cushings?

A

obesity, skin changes, psychiatric changes, glucose intolerance, thin limbs and muscle weakness, back pain due to osteoporosis and impotence or menstrual disturbances

57
Q

what happens to the skin in cushings?

A

it is thin with purple striae and bruising

58
Q

where is the obesity in cushings?

A

central, shoulders and face - moon face

59
Q

where can ACTH feed into in the HPAA?

A

directly into the adrenals

60
Q

what is the HPAA?

A

the hypothalamic-pituitary adrenal axis

61
Q

what is the process of the HPAA?

A

stress and stimuli feed into the paraventricular nucleus and then this results in excess cortisol production which feeds back to the pituitary

62
Q

what tumours is ectopic ACTH production most commonly associated with?

A

benign carcinoid tumours and small cell tumours of the lung, islet cell tumours of the pancreas, medullary carcinoma of the thyroid and tumours of the thymus gland

63
Q

what is the HPAA?

A

the hippocampus and amygdala feed into the paraventricular nucleus - the amygdala positively and hippocampus negatively. This then makes CRF which goes to the pituitary or regulation of the brain and peripheral functions for the stress response. This is also stimulated by ACTH and glucocorticoids. CRF can also go to the pituitary which makes ACTH to go to the brain or adrenal cortex to make glucocorticoids. Glucocorticoids then inhibit ACTH, CRF or the paraventricular nucleus or hippocampus.

64
Q

what are the principles of dynamic investigations?

A

whether there is excess or insufficient production there can be identical values in either circumstance. If there is excess then look to see if can be suppressed and if insufficient look to see if can be stimulated

65
Q

what is the importance of circadian rhythm in adrenals?

A

the adrenal gland contains a circadian clock that sets specific time intervals at which the adrenals most effectively respond to cortisol

66
Q

what is the diurnal rhythm of cortisol in serum?

A

the nadir cortisol levels at midnight and the peak cortisol at 8.30

67
Q

what is the nadir?

A

the lowest or most unsuccessful point

CP (38 decks)

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