FRCA Notes


Corticosteroids


  • Corticosteroids are a group of drugs whose purpose is to replicate or augment the effect of endogenous steroid hormones released by the adrenal cortex

Glucocorticoids

  • Perioperative replacement in those with adrenal suppression or insufficiency
  • Prophylaxis against PONV

  • Various acute and critical illness states
    • Septic shock: hydrocortisone 200mg/24hrs
    • Anaphylaxis: hydrocortisone 200mg
    • Exacerbation of asthma: prednisolone 40mg OD for at least 5 days
    • Exacerbation of COPD: prednisolone 30mg for 7 days
    • Bacterial meningitis: dexamethasone
    • Adrenal crisis: hydrocortisone 100mg IV stat, then 200mg/24hrs, guided by Endocrine advice
    • Myxoedema coma: hydrocortisone 100mg IV stat, guided by Endocrine advice
    • Organ donor optimisation: methylprednisolone 15mg/kg (max. 1g) stat

  • Glucocorticoid replacement in patients with adrenal insufficiency
  • Reduced mass-related clinical effects in malignancy e.g. raised ICP from intracerebral tumour, spinal cord compression: dexamethasone 16mg/24hrs in divided doses

Mineralocorticoids

  • Mineralocorticoid replacement in patients with adrenal insufficiency
  • Neuropathic postural hypotension: fludrocortisone 100-400μg/24hrs


Steroid Dose equivalent Relative glucocorticoid potency Relative mineralocorticoid potency
Hydrocortisone 100mg 1 1
Prednisolone 25mg 4 0.6
Methylprednisolone 20mg 5 0.25
Triamcinolone 20mg 5 0
Dexamethasone 3.75mg 25 0
Betamethasone 3.75mg 25 0
Fludrocortisone - 10 125
Aldosterone - 0 400


Metabolic effects

  • Gluconeogenesis (glucose synthesis from non-carbohydrate sources)
  • Stimulation of:
    • Glycogenolysis
    • Glucose release from the liver
    • Protein catabolism
  • Inhibit peripheral uptake of glucose and protein synthesis

  • In the long term:
    • Protein catabolism leads to muscle weakness and wasting, gastric mucosa weakness/susceptibility to ulceration, striae and skin thinning
    • Altered carbohydrate metabolism may cause hyperglycaemia, glycosuria and diabetes
    • Fat re-distribution to face/neck/trunk
    • Bone catabolism leads to osteoporosis

Anti-inflammatory effects

  • Reduced production of tissue transudate and cell oedema
  • Prevent macrophages and PMN's reaching inflamed tissue
  • Stimulates synthesis and augments function of lipocortin (Annexin-A1)
    • Inhibits phospholipase A2 and therefore breakdown of membrane phospholipids to arachidonic acid
    • Reduced production of inflammatory mediators (PG's, leukotrienes)

Immunnosuppressive effects

  • Depress macrophage function
  • Reduce circulating T-lymphocyte numbers
  • Reduce lymphocyte and antibody transport
  • Reduced production of IL-1 and -2
  • May lead to reactivation of TB

Vascular reactivity

  • Glucocorticoids play a permissive role in vascular smooth muscle; allow efficient response to circulating catecholamines
  • Steroid deficiency leads to ineffective response by vascular smooth muscle to catecholamines and may play a role in the requirement for vasopressors in sepsis

  • Other permissive roles:
    • Calorigenic activity of glucagon and catecholamines
    • Lipolytic effect of catecholamines
    • Bronchodilator effect of catecholamines

Adrenal suppression

  • Negative feedback on CRH and ACTH leads to adrenal atrophy
  • Adrenal cortex unable to produce glucocorticoids if:
    • Sudden cessation of exogenous glucocorticoids
    • Periods of stress e.g. surgery, infection

Fluid retention

  • Despite weak mineralocorticoid activity, glucocorticoids do act on the DCT to enact sodium retention at the expense of potassium
  • Large doses can lead to oedema, HTN and cardiac failure