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MRCP 2 > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

diagnosing and treating acromegaly

A

IGF-1
confirm with OGTT

> trans-sphenoidal resection of pituitary tumour
if surgery not appropriate:
dopamine agonist (bromocriptine, cabergoline, quinagolide, pergolide)
somatostatin analogues (ocreotide)
GH antagonist (pegvisamant)
- RTX

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2
Q

acromegaly aetiology and associations

A

95% GH secreting pituitary tumour
5% from ectopic GHRH secreting carcinoid tumour
IGF-1 secreted by liver in response to GH excess

associations:
McCune Albright
neurofibromatosis
MEN
FIPA (AIP mutation, younger)

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3
Q

causes of primary hypoadrenalism

A

Addisons (autoimmune destruction of adrenals)
TB
HIV
haemorrhage into adrenal glands
congenital adrenal hyperplasia

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4
Q

aldosterone action

A

binds to mineralocorticoid receptors in kidney
> Na retention
> K excretion

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5
Q

mechanism of secondary hypoadrenalism

A

exogenous steroids increase cortisol
> sensed by hypothalamus
> negative feedback regulation of pituitary adrenal axis to reduce secretion of corticotrophin releasing factor
> reduced levels of ACTH
> adrenal gland atrophies due to lack of stimulation

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6
Q

primary vs secondary hypoadrenalism features

A

hyperkalaemia and increased pigmentation only in primary hypoadrenalism
because ACTH is low in secondary hypoadrenalism, and there is still aldosterone secreted via RAAS

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7
Q

hypoadrenalism blood tests

A

raised urea, TSH, Ca, K
hypoglycaemia, hyponatraemia

eosinophilia
lymphocytosis
normocytic anaemia

short synacthen test:
cortisol will remain low after ACTH administration in primary (Addisons)
cortisol will rise after ACTH administration in secondary hypoadrenalism

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8
Q

hormone production in adrenals

A

cortex:
cortisol, aldosterone, DHEA
androgens

medulla:
catecholamines- adrenaline, noradrenaline, dopamine

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9
Q

adrenal cancer associated conditions

A

MEN2
Li Fraumeni
VHL
Neurofibromatosis-1
HNPCC
FAP

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10
Q

MIBG scan

A

chemical similar to adrenaline
uptaken by neuroendocrine tumour
scan 2/7 after injection

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11
Q

managing adrenal tumours

A

alpha blocker for phaeochromocytoma pre surgery

ketoconazole and metyrapone to reduce steroid
spiro to reduce aldosterone effects
mifepristone to reduce cortisol effects
tamoxifen to block oestrogen effects

mitotane CTx

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12
Q

causes of primary amenorrhoea

A

normal secondary sexual characteristics:
constitutional delay
pregnancy
GU malformations
hypo/hyperthyroid
hyperprolactinaemia
cushings
PCOS
androgen insensitivity

no secondary sexual characteristics:
primary ovarian insufficiency
CTx, RTx, autoimmune
hypothalamic dysfunction (incl weight loss, excessive exercise, chronic illness)

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13
Q

primary and secondary amenorrhoea definition

A

primary:
no menstruation by age 15y with normal secondary sexual characteristics
or no menstruation by age 13y with no secondary sexual characteristics

secondary:
no menstruation for 3-6 months with previously normal menses
or no menstruation for 6-12 months with previous oligomenorrhoea

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14
Q

oligomenorrhoea definition

A

bleeding < once per 35 days

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15
Q

amenorrhoea blood tests

A

FSH and LH- high in ovarian failure
PRL
testosterone
TSH

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16
Q

stimuli to release PTH

A

hypocalcaemia
hyperphosphataemia
low vit D

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17
Q

conversion of 25 hydroxy D3 to 1,25 hydroxyD3 is stimulated by what

A

high PTH
low PO4, low Ca

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18
Q

actions of active vitamin D

A

kidney: increased calcium and phosphate excretion
bone: increased mineralisation
small bowel: calcium and phosphate absorption

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19
Q

PTH-rP

A

acts on same receptors as PTH
secreted by tumours e.g. squamous cell, breast, kidney

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20
Q

sarcoid and vit D

A

excess production of active vit D by macrphages
> hypercalcaemia

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21
Q

familial hypocalciuric hypercalcaemia

A

auto dom
mutation in calcium receptor
does not require treatment

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22
Q

peptic ulcer from hypercalcaemia

A

due to excess gastrin

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23
Q

managing acute hypercalcaemia

A

Ca > 3
3-4L saline per day
IV bisphosphonates

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24
Q

congenital adrenal hyperplasia disorders

A

auto rec

21-hydroxylase def (cortisol +/- aldosterone def):
virilising, 70% salt losing

11-hydroxylase def (v rare):
virilising, HTN, hypokalaemia

17 hydroxylase def:
non virilising

classic- severe
non classic- milder with later onset

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25
testing for CAH
17 hydroxyprogesterone- raised in 21 hydroxylase def corticotropin stimulation test
26
CAH treatment
may not require any glucocorticoids and mineralocorticoids NaCl for infants w/ salt losing CAH antenatal steroid to reduce genital ambiguity of female infants
27
causes of Cushings syndrome
ACTH dependent: - Cushings disease (bilateral adrenal hyperplasia from pituitary adenoma secreting ACTH) - ectopic ACTH e.g. small cell lung, carcinoid - ectopic CRF (rare) ACTH independent (low ACTH from negative feedback) - steroids - adrenal adenoma/cancer - adrenal nodular hyperplasia
28
medical management of cushings
metyrapone if surgery not possibly ketoconazole no longer used due to hepato tox mitotane as adjunct CTx for adrenal cortical carcinoma
28
diagnosing cushings
phase 1: loss of diurnal variation of cortisol overnight dexamethasone suppression test 24h urinary free cortisol as alternative to dex sup test phase 2: if first line test is abnormal, do 48h low dose dex suppression test phase 3 localisation: ACTH> if detectable, do high dose dex sup test or CRH to differentiate between pituitary and ectopic > MRI pituitary/bilateral inferior petrosal sinus blood sampling if cushings disease likely > if not detectable, adrenal gland tumour is likely > CT/MRI adrenal/adrenal vein sampling
29
cushings syndrome post op
cortisol should be undetectable during recovery period will require steroids during recovery period recovery may not occur
30
Nelsons syndrome
rapidly enlarging pituitary adenoma after bilateral adrenalectomy occurs due to high ACTH from removal of neg feedback > skin pigmentation, muscle weakness, mass effects
31
causes of secondary hypogonadism
(low FSH and LH) hypogonadotropic hypogonadism tumours pituitary apoplexy marijuana haemochromatosis, sarcoid hypothyroid, hyperprolactin, diabetes, cushings
32
FSH action
stimulates sertoli cells > sperm production stimulates follicular cells > ovulation
33
hypergonadotropic hypogonadism
results from gonadal disorders elevated gonadotropins in absence of puberty at appropriate age
34
turner syndrome treatment of delayed puberty
GH and/or oxandrolone
35
IM testosterone side effects
polycythaemia
36
MODY genes
MODY1- HNF4AE MODY2- glucokinase MODY3- HNF1AE MODY 4- IPF1 MODY 5- HNF1AE
37
diagnosing T1DM
random BM > 11 and typical symptoms > same day referral c peptide or autoantibodies if doubt
38
optimum plasma glucose for self monitoring
waking: 5-7 before meals other times of day: 4-7 90 mins after meals: 4-9
39
diagnosing T2DM
asymptomatic and HbA1c > 48 or 6.5% ideally tested twice symptomatic and one abnormal HbA1c fasting glucose 7 or more if Hba1c not appropriate e.g. pregnancy, children, T1DM, haemaglobinopathy
40
impaired glucose tolerance and impaired fasting glucose
OGTT 7.8-11.1 > IGTT fasting BM 5.6-7 > impaired fasting glucose fasting BM 7 or more > diabetes
41
T2DM management
1. metformin 2. add gliptin or sulfonylurea or SGLT2i 3. consider triple therapy 4. consider change to GLP1 mimetic or insulin
42
causes of diabetes insipidus
cranial: idiopathic craniopharyngiomas trauma pituitary surgery lymphocytic hypophysitis dysgerminomas infiltrative process of hypothalamus e.g. sarcoid renal: x linked/dom ADHr abnormality (childhood onset) hypercalcaemia, hypokalaemia renal disease demeclocycline, lithium
43
when to start dextrose with DKA pt
when glucose < 14
44
DKA indications for ITU/HDU
low GCS hypokalaemia ketones > 6 pH < 7.1
45
gigantism
acromegaly before puberty increased height is main features
46
hyperaldosteronism
hypokalaemia, HTN, normal or mild hypernatraemia - Conns > surgery - adrenocortical hyperplasia > spiro or amiloride
47
causes of hyperaldosteronism
Primary, low renin: conn syndrome (aldosterone producing adenoma) b/l adrenocortical hyperplasia adrenal carcinoma, GRA secondary, high renin (due to renal hypoperfusion): renal artery stenosis accelerated HTN CCF or hepatic failure coarctation aorta
48
what drugs might affect renin/aldosterone tests?
ACEi spironolactone CCBc ARB
49
treating hyperaldosteronism
adrenocortical hyperplasia > spiro or amiloride GRA > dex for 4/52 conn> lap adrenelectomy
50
causes of hyperparathyroidism
primary: adenoma hyperplasia cancer secondary: CKD low vit D tertiary: after prolonged secondary hyperparathyroidism, seen in CKD
51
drug causes of hypercalcaemia
lithium thiazides
51
tertiary hyperparathyroidism
glands do not respond to normal feedback occurs after prolonged secondary hyperparathyroidism glands continue to produce excessive PTH though hypocalcaemia has been treated
51
primary vs secondary vs tertiary hyperparathyroid
primary: hypercalcaemia hypophosphataemia PTH raised or normal secondary: hypocalcaemia high PO4 in renal disease raised PTH tertiary: hypercalcaemia high PTH PO4 often raised
52
predominantly increased TGs vs cholesterol
TG: alcohol, obesity, T2DM CKD, liver disease high dose oestrogens, pregnancy retinoids, beta blockers, thiazides cholesterol: smoking hypothyroid nephrotic syndrome, renal transplant cholestasis
53
when to refer hypertriglyceridaemia
TG > 10 urgently if TG > 20 (if not due to poor glycaemic control or alcohol) non HDL > 7.5 total cholesterol > 9
54
lipid lowering drugs side effects
simvastatin- potentiates warfarin and digoxin gemfibrozil- absorption impaired by anion exchange resins gemfibrozil and bezafibrate- potentiate warfarin ezetimibe- headache, abdo pain, thrombocytopaenia, myositis, pancreatitis, abnormal lfts anion exchange resins- abnormal lfts, impaired absorption of dig, warfarin, thyroxine, fat soluble vits probucol- eosinophilia, long qt
55
whipple's triad
non diabetic hypoglycaemia - clinical symptoms - BM< 3.3 - resolution of symptoms after glucose is corrected
56
causes of non diabetic hypoglycaemia
insulin, sulfonylureas GH or adrenal insufficiency (hypopituitarism or addisons) hyperthyroid malnutrition, alcohol insulinoma, fibroma, sarcoma, renal cell ca (IGF 1 secretion) large liver tumours (increased gluc consumption) nesidioblastosis, islet hypertrophy beta blockers, fluoroquinolones, heparin, ppi, sulfonylureas, tramadol, quinine, haloperidol
57
what is released in response to hypoglycaemia
GH cortisol glucagon adrenaline
58
inflammatory and infiltrative causes of hypopituitarism
lymphocytic hypophysitis haemochromatosis sarcoid, TB, langerhand histiocytosis ipilumab, tremelimumab
59
presentation of pituitary apoplexy
sudden onset headache, visual changes and ophthalmoplegia palsies of CN III, IV, VI
60
secondary hypothyroidism
low T3, T4 due to reduced TSH pituitary cause
61
c peptide hyperinsulinaemia
low in exogenous high in endogenous
62
liddle syndrome
auto dom dysfunctional Na channels in collecting duct HTN, hypokalaemic metabolic alkalosis, hypernatraemia appears like primary hyperaldosteronism but renin and aldosterone are suppressed
63
indications for FSH testing to diagnose menopause
> 45y with atypical symptoms 40-45y with menopausal symptoms and change in cycle < 40y if menopause suspected
64
MEN
MEN1: Parathyroid, Pituitary, Pancreas auto dom, 11q13 MEN2A: Parathyroid, Phaeochromocytoma, Medullary thyroid auto dom, RET 10q11.12 MEN2B: Phaeochromocytoma, Medullary thyroid, Marfinoid, Mucosal neuromas auto dom, RET
65
diagnosing medullary thyroid ca
raised calcitonin
66
should you biopsy a suspected phaeochromocytoma?
no
67
familial phaeochromocytoma conditions
MEN (usually bilateral) neurofibromatosis VHL
68
phaeochromocytoma triad
headache palpitations sweating
69
phaeochromocytoma catecholaminergic effects
alpha: - increased BP and cardiac contractility - gluconeogenesis, glycogenolysis - intestinal relaxation beta: - increased HR and contractility
70
consequences of hyperinsulinaemia in PCOS
- reduced hepatic DHBG > increased free T - increased androgen production > anovulation, oligo/amenorrhoea - weight gain
71
blood tests in PCOS
T may be high high LH:FSH raised HbA1c normal to low SHBG PRL may be mildly elevated
72
drug treatment for premature ejaculation
dapoxetine SSRI
73
turner syndrome cardiac problems
bicuspid aorta coarctation partial anomalous venous drainage
74
chemo for thyroid ca
tyrosine kinase inhib lenvatinib and sorafenib for locally advanced or metastatic differentiated cancer if radioiodine did not work cabozantinib for medullary ca that has spread or not operable
75
phases of thyroid eye disease
active- 6-24 months inactive- chronic fibrotic phase, further changes are unlikely but proptosis remains
76
when to admit or get urgent advice for thyroid eye disease
dysthyroid optic neuropathy (reduced acuity or colour discrimination) history of globe subluxation risk of corneal ulceration (sclera or cornea visible when eyes are closed)
77
radioiodine uptake in thyroxoticosis
increased or normal uptake: Graves toxic multinodular toxic/hot nodule reduced uptake: excess thyroxine ingestion thyroiditis (dequervains, post partum, silent) ectopic thyroid tissue iodine administration
78

MRCP 2 (12 decks)

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