Endocrine Flashcards
(38 cards)
Carbimazole
- Thionamide (antithyroid drug)
- drug of choice
- prodrug; converted to the active metabolite thiamazole via first pass metabolism
- has immunosuppressive properties and thus is useful in the treatment of Graves’ disease
- some serious side effects (agranulocytosis, skin aplasia, rash, nausea, vomiting)
propiothiouracil (PTU)
- Thionamide (antithyroid drug)
- Less active and shorter half life than carbimazole so twice the dosing is required.
- PTU usually second line.
- reduces the conversion of T4 → T3 peripherally giving some more acute effects.
- better safety data in pregnancy
Propanolol
- beta blocker
- used for symptomatic treatment in hyperthyroidism
- do not affect hormone levels
Potassium Iodide
- antithyroid drug
- Reduces thyroid hormone release acutely, used in thyroid storm and pre-operatively
levothyroxine
- synthetitc T4 used to treat hypothyroidism
- Generally need 1.7-2.0 micrograms / kg / day (with no gland whatsoever)
- Best taken on an empty stomach
- Avoid taking with proton pump inhibitors, ferrous sulphate or calcium
- Start lower, especially in elderly and in cardiac disease
- Increased thyroxine increases the load on the heart
Cabergoline
- Dopamine agonist (D2 receptor agonist)
- treatment of prolactinoma
- Most commonly used, well tolerated
- Long half-life, therefore only requires once/twice weekly dosing
- Also used to treat parkinson’s (but higher doses)
- Association with cardiac fibrosis
- Echocardiogram at the start of treatment to determine if there is any fibrosis
Quinagolide
- Dopamine agonist
- treatment of prolactinoma
Bromocriptine
- Dopamine agonist
- treatment of prolactinoma
Thionamides
Reduce thyroid hormone synthesis
o Inhibit iodide oxidation
o Inhibit iodination of tyrosine
o Inhibit coupling of iodotyrosines
- T4 has a long half-life (7 days) and therefore treatment with antithyroid drugs can take from 10-20 days for any clinical benefit to be seen.
Hydrocortisone
- cortisol replacement therapy
- used in adrenal insufficiency
- treatment is initially empirical, as waiting could be fatal
- Metabolised to cortisol. Most physiological way of replacing cortisol
- If unwell, give intravenously first
- Then 15-30mg oral tablets daily in divided doses (for long-term maintenance)
- Try to mimic diurnal rhythm
- Highest levels in the morning, therefore give higher dose in the morning
patient education is important:
- ‘sick day rules’ – double oral hydrocortisone for 3 days when unwell
- Cannot stop suddenly, as this will cause adrenal crisis
- Need to wear identification
Fludrocortisone
- aldosterone replacement therapy for primary adrenal insufficiency
- not used for secondary insufficiency because aldosterone is regulated by RAAS, not the pituitary
- Careful monitoring of BP and plasma potassium to determine the adequacy of replacement
Metyrapone/ketoconazole
- Inhibit cortisol production, but not very well
tolerated - Short term measure for treating cortisol excess
spironolactone
- Competitive antagonist at MR, androgen and progesterone receptors
- Unwanted side effects gynaecomastia, hyperkalaemia
- Management of Primary Aldosteronism
eplerenone
- Selective MR antagonist, no observed anti-androgen effects
- Management of Primary Aldosteronism
amiloride
- blocks ENaC, therefore blocks effect of
aldosterone - Management of Primary Aldosteronism
PHAEOCHROMOCYTOMA pre-operative treatment
- α1 +/- β1 antagonists to block effects of catecholamine surge
- Can become haemodynamically unstable in surgery if this is not done
fludrocortisone
- aldosterone replacement therapy
- used for primary adrenal insufficiency
Hydrocortisone
- cortisol replacement therapy
- used for primary and secondary adrenal insufficiency
- Metabolised to cortisol. Most physiological way of replacing cortisol
- dosing aims to mimic diurnal rhythm
Tamsulosin
- alpha 1 antagonist
- causes relaxation of smooth muscle in BPH
Treatment of hypercalcaemia
1) bisphosphonates - inhibit osteoclasts
2) calcitonin - given as a SC injection, opposes the action of PTH but only effective for 48 hours
3) glucocorticoid therapy - inhibits vitamin D production
4) if primary hyperparathyroidism and resistant to treatment - parathyroidectomy
Biguanides
Metformin
Mimic action of insulin by suppressing hepatic gluconeogenesis.
Inhibits PEPCK and G6Pase
sulphonylureas
gliclazide, glipizide, glibenclamide
block ATP-dependent K+ channel, increasing insulin release
May predispose to hypoglycaemia
Associated with weight gain
Thiazolidinediones
pioglitazone
stimulate expression of genes involved in triglyceride
storage.
o PPARγ agonists
o increase transcription of insulin sensitising genes
Stop inappropriate deposition of lipid in non-adipose tissues (which leads to insulin resistance) – improves insulin sensitivity
Associated with weight gain
The incretin effect
Observation that more insulin is released when glucose is ingested orally as opposed to injected.
Dependent on incretins - gut hormones that sensitize beta cells to stimulate more insulin release
o Glucagon-like peptide-1 (GLP-1)
o Gastric inhibitory peptide (GIP)
Rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4).
