Mineralocorticoi
Chapter 6 – Endocrine Glucocorticoid SEs
d SEs
System - Avascular necrosis of
2+
- Ca loss femoral head
- Hypertension - Diabetes
ANTIDIURETIC HORMONE DISORDERS - K+ loss - Muscle wasting
Diabetes insipidus - Na+ retention - Osteoporosis
- Water - Peptic ulceration and
Vasopressin and desmopressin (ADH) retention perforation
Used to treat pituitary diabetes insipidus - Psychiatric reactions
Dose is tailored to produce diuresis every
24hrs to avoid water intoxication Managing side effects
Desmopressin = more potent and has a Use lowest effective dose for shortest time
longer duration of action but doesn’t have a Suppressive action of corticosteroid on
vasoconstrictor effect. cortisol secretion is least when given as
single dose in the morning
ADH antagonists In children < 15 years, use large-volume
Demeclocycline = used to treat hyponatraemia spacer devices to administer inhaled CS =
due to inappropriate ADH secretion, if fluid increased airway deposition and reduced
restriction alone doesn’t restore [Na] oropharyngeal deposition
CORTICOSTEROID RESPONSIVE Replacement Therapy
CONDITIONS Adrenal cortex – secretes hydrocortisone
(cortisol) which has glucocorticoid activity
Corticosteroids: General use
and weak MC activity. Also secretes
Fludrocortisone – mineralocorticoid activity
aldosterone
allows use in postural hypotension in
autonomic neuropathy
1. In deficiency states – physiological
Dexamethasone and betamethasone – long
replacement is best achieved using
duration allows use against corticotropin
hydrocortisone + fludrocortisone
secretion in congenital adrenal hyperplasia
2. In Addison’s or post-adrenalectomy – use
Glucocorticoids – suppressive action on
oral hydrocortisone (2 doses – larger in the
hypothalamic-pituitary-adrenal axis is
morning and smaller in the evening)
greatest and prolonged when given ON
3. In acute adrenocortical insufficiency – use
MHRA/CHM: rare risk of central serous IV hydrocortisone every 6-8 hours
chorioretinopathy with local and systemic use 4. In hypopituitarism – give glucocorticoids as
– reported after use in inhaled, intranasal, in adrenocortical insufficiency. Depending
epidural, intra-articular, topical dermal and on pattern of hormone deficiency, give
periocular routes. Report any blurred vision or levothyroxine and sex hormones
visual disturbances
MC SEs are greatest with fludrocortisone
followed by hydrocortisone, corticotropin and
tetracosactide. Negligible actions with high
potency glucocorticoids, betamethasone,
dexamethasone, methylprednisolone,
Glucocorticoid therapy
prednisolone and triamcinolone
, Chapter 6 – Endocrine System
Hydrocortisone – unsuitable for long-term If BG falls to < 4mmol/L or warning signs of
disease suppression but can be used for hypoglycaemia develop, do not drive. If
adrenal replacement therapy already driving:
Prednisolone and deflazacort – mainly GC o Stop vehicle in safe place
activity o Switch off engine, remove keys from
Betamethasone and dexamethasone – long ignition and move from driver’s seat
DoA but poor MC action hence suitable for o Eat or drink suitable source of sugar
corticotrophin suppression o Wait until 45mins after BG has
normalised, before continuing drive
Prednisolone 5mg – equivalent doses If hypoglycaemia awareness has been lost,
= hydrocortisone 20mg do not drive and inform DVLA
= deflazacort 6mg
= prednisolone 5mg Alcohol
= methylprednisolone 4mg This can make signs of hypoglycaemia less
= triamcinolone 4mg clear and cause delayed hypoglycaemia
= betamethasone 750 micrograms Drink alcohol in moderation and with food
= dexamethasone 750 micrograms
Oral glucose tolerance tests (OGTT) – measures
CUSHING’S SYNDROME AND DISEASE [blood glucose] after fasting and then 2 hours
after drinking a standard anhydrous glucose
Most types are treated surgically drink (or Polycal or Rapilose OGTT oral solution)
Metyrapone – used to control symptoms Mainly used for diagnosis of impaired
Ketoconazole – has a direct effect on glucose tolerance. It’s not recommended or
corticotropic tumour cells necessary for routine diagnostic use in
DIABETES MELLITUS severe hyperglycaemia symptoms
In Pts with milder symptoms and a [BG]
Persistent hyperglycaemia caused by doesn’t establish/exclude DM – use OGTT
deficient insulin secretion or by resistance
to insulin = abnormalities of carb, fat and HbA1c (Glycated haemoglobin) - forms when
protein metabolism RBCs are exposed to glucose in the plasma
Gestational = develops during pregnancy HbA1c test – reflects average plasma
and resolves after delivery glucose over previous 2-3 months and
Secondary = caused by pancreatic damage, provides a good indicator of glycaemic
hepatic cirrhosis or endocrine disease control. It can be
performed at any mmol/mol %
Driving time of the day and 42 6
All insulin Pts must inform DVLA doesn’t require any 48 6.5
Avoid hypoglycaemia and be aware of special prep e.g. 53 7
fasting 59 7.5
warning signs and actions to take
Mmol/mol = mmol 64 8
Insulin Pts should always carry a glucose
of glycated 69 8.5
meter and BG strips when driving
75 9
Drivers must check their BG at least 2 hours haemoglobin per
before and every 2 hours while driving mol of haemoglobin
BG should be >5mmol/L when driving
If BG falls to < 5mmol/L, eat a snack.
Avoid HbA1c in:
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