Endocrinology Flashcards
Management nephrogenic diabetes insipidus
thiazides
low salt and protein diet
Management central diabetes insipidus
desmopressin
define cranial diabetes insipidus
deficiency of ADH
define nephrogenic diabetes insipidus
insensitivity to ADH
Causes of cranial diabetes insipidus
- idiopathic
- head injury
- pituitary surgery
- craniopharyngioma
- histocytosis X
- DIDMOAD - DI + DM + Optic atrophy + deafness = Wolfram’s syndrome
- haemochromatosis
Causes of nephrogenic diabetes insipidus
- genetic
- electrolytes imbalance (hypercalcaemia, hypokalaemia)
- drugs (demeclocycline, lithium)
- tubulo-interstitial disease (obstruction, sickle cell, pyelonephritis)
Fts of diabetes insipidus
polyuria
polydipsia
Investigation + result in diabetes insipidus
- high plasma osmolality
- low urine osmolality (<700)
- water deprivation test (12hrs no water + vasopressin - if response it is central DI)
1st line management of T2DM
diet and lifestyle advice
single drug manaement T2DM
metformin
if CI =
- if CVD established/risk orCHF = SGLT-2i
- otherwise = any other
Troubleshooting intolerance to metformin
- titrate up slowly
- trial MR
When to use GLP-1 mimentic (i.e semaglutide/ozempic)
does not achieve HbA1c control on dual drug therapy AND
- BMI >35
- BMI <35 but insulin would have implications/weight loss would benefit comorbidities
AND only continued if reduction of at leasr 11mmol/mol AND weight loss 3% in 6mo
NOT additional to insulin unless under specialist care
when to start 3rd line management T2DM
if HbA1c >58mmol/mol + with lifestyle advice and one drug
Second drug management T2DM
- if high risk/established CVD or HF - SGLT-2 inhibitor
- sulfonylurea if no risk of hypoglycaemia
- DPP4-i or thiazolidindedione if at risk of hypoglycaemia
target HbA1c if on lifestyle + sulfonylurea
53
target HbA1c if on one drug but HbA1c has rised to 58mmol/mol
53mmol/mol
target HbA1c if on lifestyle + one drug (excluding sulfonylurea)
48mmol/mol
Typical blood findings seen along with Cushing’s syndrome
hypokalaemic metabolic alkalosis (esp a/w ectopic ACTH in SCC)
impaired glucose tolerance
3 most common tests used to confirm Cushing’s syndrome
- overnight (low-dose) dexamethasone suppression = most sensitive; positive = no cortisol spike in am
- 24hr urinary free cortisol (2 measurements)
- bedtime salivary cortisol 2 measuremetns required)
Localizing tests for Cushing’s syndrome
1. fist line test
2. interpretation
- 9am and midnight plastma ACTH (and cortisol)
- ACTH suppressed = non-ACTH dependent cause (i.e adrenal adenoma)
Localizing tests for Cushing’s syndrome
1. second line test
2. interpretation
- High dose dexamethasone supression test
- cortisol not supp BUT ACTH supp = non-ACTH dependent (o.e adrenal adenoma)
- cortisol AND ACTH supp = Cushing’s disease (pituitary adenoma)
- cortisol AND ACTH not supp = ectopic ACTH
investigations for suspected Addison’s disease
1. in GP
2.2nd line GP/hospital
- 9am serum cortisol (if >500 Addison very unlikely)
- ACTH simulation (short Synacthen test) = plasma cortsol before and 30 mins after giving Synachen 250ug IM
associated electrolyte abnromalities with Addison’s disease (undiagnosed)
hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis
