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Year 4 > Endocrinology 2 > Flashcards

Endocrinology 2 Flashcards

1
Q

what is anterior pituitary made of?

A

develops from rathke’s pouch (upgrowth of ectoderm from primitive oral cavity)

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2
Q

what is posterior pituitary made of?

A

..

neural crest origin

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3
Q

anterior pituitary hormones?

A

FLAT PIG

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4
Q

posterior pituitary hormones?

A

ADH

oxytocin (squeezes milk out of breast ducts)

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5
Q

anterior pituitary dysfunction phenotype?

A

relates to hormones which are reduced

often more than one hormone lost and also structural effects of large tumour (adenoma) bulk

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6
Q

tumour in pituitary?

A

basically all are adenomas
mostly adenoma of one cell type (eg prolactinoma, ACTH producing cells etc)
can also have craniopharyngioma, cerebral and secondary tumours

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7
Q

causes of hypopituitarism?

A 
tumours
vascular (sheehans, severe hypotension)
infection
hypothalamic disorder
iatrogenic (radiation, hypophysectomy)
miscellaneous (sarcoidosis, haemochromatosis)
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8
Q

hypothalamic disorders?

A

tumours
functional disorders
isolated deficiency of GNRH and LH/FSH

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9
Q

hypopituitarism usually presents late, when will it present early?

A

pre-menopausal women as they get amenorrhoea

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10
Q

structural effects of pituitary tumour?

A

can press on surrounding structures (chiasm ect)
headache
invasion of cavernous sinus
CSF leak due to invasion

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11
Q

effects of tumours pressing on optic chiasm?

A

bitemporal hemianopia

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12
Q

order in which hormones are lost?

A 
GGAT
gonadotrophins
GH
ACTH
TSH
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13
Q

functional effects of pituitary tumour?

A 
loss of normal hormone function
-
-
-
-
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14
Q

LH and FSH should be high or low in post menopausal women?

A

high

if theyre low, might be pituitary problem

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15
Q

biochemistry of hypopituitarism?

A

measure specific hormones

  • TSH and T4 (both would be low)
  • LH/FSH (both low)
  • oestrogen/testosterone
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16
Q

why arent GH and cortisol useful to measure?

A

released in pulsatile manner and very variable levels

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17
Q

biochemical tests for hypopituitarism (cortisol and GH)?

A

hormones are low so try and stimulate them

- make patient hypoglycaemic to stress body and stimulate cortisol production (insulin tolerance test)

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18
Q

imaging in hypopituitarism?

A

MRI

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19
Q

anterior pituitary deficiency usually involves multiple hormones, is excess the same?

A

no

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20
Q

how can FSH and LH be measured?

A

FSH and LH in blood

oestrogen and testosterone in blood

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21
Q

clinical effects of FSH and LH excess?

A

none really

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22
Q

ACTH excess?

A

causes excess cortisol production at adrenals (cushings)

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23
Q

symptoms of cushings?

A 
moon face
weight gain (central)
thin limbs
buffalo hump
thin hair and skin (poor wound healing)
frontal balding
aggressive striae
diabetes (polyuria) as cortisol is an insulin antagonist
hypertension
proximal myopathy
acne
easy bruising
osteoporosis 
oligomenorrhoea
headaches
insomnia
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24
Q

most common cause of cushings phenotype?

A

excess steroid medication

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25
Q

other causes of cushings?

A

tumours/hyperplasia in adrenal cortex
ectopic ACTH
pituitary tumour

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26
Q

cushings biochemistry test?

A

dexamethasone suppression test (body should recognise extra steroid and switch off cortisol production in normal people)

27
Q

how is MSH involved in cushings?

A

anything that increases ACTH also increases MSH production as theyre from the same precursor

28
Q

features of MSH excess?

A

pigmentation

in old scars and in buccal mucosa

29
Q

how is dexamethasone suppression test done?

A

1mg given at night then early morning blood test next day (cortisol should be <50 in normal people)
- also look at ACTH next day

30
Q

if cortisol is high but ACTH is low, what does this indicate?

A

primary adrenal problem

31
Q

if cortisol not suppressed what other test done??

A

////

32
Q

where would you look for a cause if cortisol and ACTH are both high?

A

pituitary (MRI)

if ACTH ridiculously high then do CXR to look for a malignancy

33
Q

why is dynamic testing (eg dexamethasone suppression) not needed for thyroid?

A

hormones are very steady

34
Q

function of prolactin?

A

breast milk production

35
Q

prolactin excess phenotype?

A

galactorrhoea
gynaecomastia a little (not as much as in oestrogen excess)
loss of libido and erectile dysfunction
amenorrhoea

36
Q

most common pituitary tumour?

A

prolactinoma

37
Q

types of prolactinoma?

A

micro (<1cm) = benign, doesnt reallt cause problems

macro (>1cm) = tend to grow and can cause problem

38
Q

how can you tell whether micro or macro?

A

do MRI 6 months apart and look at growth

39
Q

what drugs are used in prolactinoma?

A

dopamine agonists (cabergoline = first line, also bromocriptine and quinagolide)

40
Q

why is dynamic testing not needed in prolactinoma?

A

prolactin only present physiologically in pregnancy and lactation
so measuring prolactin levels is enough to detect a problem

41
Q

why do dopamine agonists work in prolactinoma?

A

dopamine inhibits prolactin so can shrink the tumour

42
Q

management of micro vs macro prolactinoma?

A

all need dopamine agonist

only the macro might need surgery in certain cases

43
Q

what does GH excess cause?

A

acromegaly

44
Q

features of acromegaly?

A 
big hands and feet
prominent brow
large tongue
prominent jaw
spacing between teeth
can get hepatosplenomegaly
can get large heart
bone overgrowth causing premature arthritis
sweating
diabetes 
hypertension
polyps (need to screen for cancer)
45
Q

what happens if theres GH excess before epiphyseal fusion in childhood?

A

giantism

46
Q

biochem test for acromegaly?

A

need dynamic testing
glucose tolerance test (should suppress GH in normal people)
can also measure IGF-1 which is more stable

47
Q

imaging for GH excess?

A

pituitary MRI

48
Q

management of pituitary adenoma?

A

prolactinoma = medical
trans sphenoidal surgery for others
radiotherapy can be used to debulk if surgery doesnt get it all

49
Q

too much ADH?

A

SIADH

50
Q

too little ADH?

A

diabetes insipidus

51
Q

types of diabetes insipidus?

A

cranial

nephrogenic (kidney cant respond to ADH)

52
Q

how does ADH work?

A

goes to kidney >distal convoluted tubule > attracts aquaporin 2 channels to the membrane to allow water resorption
works via cAMP

53
Q

diabetes insipidus phenotype?

A

polyuria (clear urine)

polydipsia

54
Q

how is diabetes insipidus diagnosed?

A

water deprivation test (ADH v difficult to measure)
dont allow them to drink between 8am and 4pm and continuously measure blood and urine osmolality (urine will stay dilute and blood will increase osmolality)
then at 4pm give artificial ADH (urine will immediately concentrate in cranial DI)

55
Q

diabetes insipidus bloods?

A

high osmolality (disconnect between high osmolality blood but still dilute urine)

56
Q

psychogenic DI?

A

excessive water drinking which eventually flushes out concentration gradient in kidney?

57
Q

management of cranial DI?

A

ADH/vasopressin

titrate dose to plasma sodium level and symptoms

58
Q

management of nephrogenic DI?

A

difficult
correct reversible causes (hyperkalaemia, hypercalcaemia, stop lithium)
massive doses of ADH can sometimes help
generally just need to drink loads and loads

59
Q

causes of SIADH?

A 
neoplastic
pulmonary infection
CNS problems
drugs (too much desmopressin, some psychiatric drugs)
idiopathic
hereditary
60
Q

how is SIADH diagnosed?

A

low plasma osmolality

high urine osmolality

61
Q

SIADH phennotype?

A

confusion
lethargy
nomovolaemic
symptoms of underlying cause

62
Q

biochem of SIADH?

A

low plasma sodium
low plasma osmolality
inappropriate high urine osmolality
inappropriate high urine sodium

63
Q

how is SIADH managed?

A

water restriction (1-1.5L per day)
not pleasant for patient
if fluid restriction doesnt work, can use demeclocycline (uncouples aquaporin 2 receptor)
tolvaptan (V2 receptor antagonist allows free water excretion)

64
Q

why dont diuretics work in SIADH?

A

also cause loss of sodium etc therefore there is no change in osmolality

Year 4 (83 decks)

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