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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
other causes of cushings?
tumours/hyperplasia in adrenal cortex ectopic ACTH pituitary tumour
26
cushings biochemistry test?
dexamethasone suppression test (body should recognise extra steroid and switch off cortisol production in normal people)
27
how is MSH involved in cushings?
anything that increases ACTH also increases MSH production as theyre from the same precursor
28
features of MSH excess?
pigmentation | in old scars and in buccal mucosa
29
how is dexamethasone suppression test done?
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
if cortisol is high but ACTH is low, what does this indicate?
primary adrenal problem
31
if cortisol not suppressed what other test done??
////
32
where would you look for a cause if cortisol and ACTH are both high?
pituitary (MRI) | if ACTH ridiculously high then do CXR to look for a malignancy
33
why is dynamic testing (eg dexamethasone suppression) not needed for thyroid?
hormones are very steady
34
function of prolactin?
breast milk production
35
prolactin excess phenotype?
galactorrhoea gynaecomastia a little (not as much as in oestrogen excess) loss of libido and erectile dysfunction amenorrhoea
36
most common pituitary tumour?
prolactinoma
37
types of prolactinoma?
micro (<1cm) = benign, doesnt reallt cause problems | macro (>1cm) = tend to grow and can cause problem
38
how can you tell whether micro or macro?
do MRI 6 months apart and look at growth
39
what drugs are used in prolactinoma?
dopamine agonists (cabergoline = first line, also bromocriptine and quinagolide)
40
why is dynamic testing not needed in prolactinoma?
prolactin only present physiologically in pregnancy and lactation so measuring prolactin levels is enough to detect a problem
41
why do dopamine agonists work in prolactinoma?
dopamine inhibits prolactin so can shrink the tumour
42
management of micro vs macro prolactinoma?
all need dopamine agonist | only the macro might need surgery in certain cases
43
what does GH excess cause?
acromegaly
44
features of acromegaly?
``` 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
what happens if theres GH excess before epiphyseal fusion in childhood?
giantism
46
biochem test for acromegaly?
need dynamic testing glucose tolerance test (should suppress GH in normal people) can also measure IGF-1 which is more stable
47
imaging for GH excess?
pituitary MRI
48
management of pituitary adenoma?
prolactinoma = medical trans sphenoidal surgery for others radiotherapy can be used to debulk if surgery doesnt get it all
49
too much ADH?
SIADH
50
too little ADH?
diabetes insipidus
51
types of diabetes insipidus?
cranial | nephrogenic (kidney cant respond to ADH)
52
how does ADH work?
goes to kidney >distal convoluted tubule > attracts aquaporin 2 channels to the membrane to allow water resorption works via cAMP
53
diabetes insipidus phenotype?
polyuria (clear urine) | polydipsia
54
how is diabetes insipidus diagnosed?
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
diabetes insipidus bloods?
high osmolality (disconnect between high osmolality blood but still dilute urine)
56
psychogenic DI?
excessive water drinking which eventually flushes out concentration gradient in kidney?
57
management of cranial DI?
ADH/vasopressin | titrate dose to plasma sodium level and symptoms
58
management of nephrogenic DI?
difficult correct reversible causes (hyperkalaemia, hypercalcaemia, stop lithium) massive doses of ADH can sometimes help generally just need to drink loads and loads
59
causes of SIADH?
``` neoplastic pulmonary infection CNS problems drugs (too much desmopressin, some psychiatric drugs) idiopathic hereditary ```
60
how is SIADH diagnosed?
low plasma osmolality | high urine osmolality
61
SIADH phennotype?
confusion lethargy nomovolaemic symptoms of underlying cause
62
biochem of SIADH?
low plasma sodium low plasma osmolality inappropriate high urine osmolality inappropriate high urine sodium
63
how is SIADH managed?
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
why dont diuretics work in SIADH?
also cause loss of sodium etc therefore there is no change in osmolality

Year 4 (83 decks)

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