Steroid abnormalities Flashcards
Vitaligo
Autoimmune antibodies against melanocytes
Patches of loss of skin pigmentation
What typical symptoms indicates both mineralocorticoid (aldosterone) and glucocorticoid (cortisol) deficiency?
Hyponatraemia and hypotension
Typical symptoms of mineralocorticoid deficiency
Hyponatremia - Aldosterone retains Na+ and water therefore leading to secondary ADH secretions
Hypotension - Due to Na+ loss
HYPERKALEMIA IN MINERALOCORTICOID DEFICIENCY - Due to decreased K+ secretions from aldosterone
Metabolic acidosis (failure for kidney to secrete H+)
Typical symptoms of glucocorticoid deficiency
Hyponatremia - Loss of cortisol inhibition of ADH
Hypoglycaemia - Loss of gluconeogenesis and glycogenolysis induced by cortisol
Hypo-tension Loss of cortisol effect on vascular tone
Causes of adrenal failure
Primary
- Adrenal gland dysfunction
Secondary
- Pituitary/ hypothalamus problem
Primary adrenal failure symptoms and pathophysiology
GOOD TAN
- No cortisol production
- Tf no negative feed back on hypothalamus ACTH release
- ACTH is peptide product of POMC
- POMC produces melanocyte stimulating hormone MSH
- MSH causes good tan
What are key observations to make with a child facing increasing obesity.
1) Change in appearance over time
If slow - then exogenous (eat too much) and not serious
If sudden - pathological
2) Growth pattern
- If no growth (short stature) then pathological (glucocorticoid excess)
3) Other features suggesting pathological causes
Other features of glucocorticoid excess
- Moon face
- Thinned skin:
- Facial plethora (glowing face)
- Violaceous striae
- bruising
- Androgen excess as cortisol is in path of making androgens
- Hirsutism
- Amennorrhoea
Myopathy
Hypertension
Glucose intolerance
Why do some patients present with hyperaldosteronism symptoms on top of typical glucocorticoid excess sympotoms?
Cortisol binds with equal affinity to MC and GC receptors. but is normally metabolised before binding to MC receptors.
In pathological conditions where there is excess cortisol produced by adrenal glands this excess overrides the cortisol metabolism.
Differentials of glucocorticoid excess
- Primary adrenal tumor
- ACTH secreting tumors
- Pituitary or ectopic - Exogenous GC’s
What do you get with partial loss of glucocorticoid receptors?
Inc. in ACTH as the hypothalamus’ deficient GC receptors does not read there is sufficient cortisol circulating so no negative feed back.
Therefore excess cortisol is produced causing typical symptoms of GC and MC excess.
SECONDARY MC EXCESS SYMPTOMS
- Hyper-androgenism
- Fatigue/ tiredness - cortisol insensitivity when sick
What do you get with loss of MC receptors?
Mineralocorticoid resistance
(Pseudohypoaldosteronism)
- Can’t retain Na+ so HYPONATREMIA
- Fails to excrete K+ and H+ so HYPERKALEMIA and ACIDOSIS.
Loss of ACTH receptors?
High ACTH as no receptors to act on
Severely low cortisol levels - Adrenal crisis (bad!!