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REGUB: Adrenal & Parathyroid Pathology (i) (Hypercortisolism (clinical…
REGUB: Adrenal & Parathyroid Pathology (i)
Pure endocrine organs
pit
thyroid
parathyroid
adrenal
Endocrine components in mixed organs
pancreas
ovary
testis
endocrine disease usually comes to attention via...
hyperfunction
hypofunction
enlargement - mass effect
Adrenal gland
medulla: centre, dark brown
cortex
lighter periphery
surrounded by capsule
divided into...
zona glomerulosa - outermost, mineralocorticoids (aldosterone)
zona fasciculata - some glucocorticoids (cortisol)
zona reticularis - innermost, most of cortisol + sex steroids
adrenocortical hyperfunction: hypercortisolism, hyperaldosteronism, adrenogenital syndromes
chol = precursor to adrenal hormones (CoA reductase enzyme necessary), then pregnelone
Hypercortisolism
aka Cushing's syndrome
increased glucocorticoid levels
exogenous
iatrogenic
admin of glucocorticoids
most common cause
results in adrenal atrophy - hence NB to titre off slowly
endogenous
primary hypothal-pit diseases
increased ACTH in 70-80%
causes adrenal hyperplasia
e.g. pit adenoma (Cushing disease)
adrenal causes
adenoma
carc
nodular hyperplasia (10-20% of cases)
paraneoplastic
ectopic ACTH by a neoplasm (e.g. SCLC, carcinoid tumours, medullary carc of thyroid, islet cell tumours)
morphology of adrenal gland depends on cause
clinical features
HTN
weight gain (truncal obesity, buffalo hump)
moon face
decreased muscle mass (due to atrophy of fast twitch myofibres) - thin limbs
hyperglycaemia (increased gluconeogenesis, inhibited uptake of glucose by cells) - glycosuria + polydipsia
fragile thin skin (catabolic effect of cortisol on protein in skin - loss of collagen), easy bruising, striae
osteoporosis (induced bone resorption)
immunosuppression (infections)
mental disturbances
mood swings
depression
psychosis
hirsutism
menstrual abnormalities
Dx
24hr urine collection for cortisol
only small amount in urine (most bound to proteins in blood) - flare -ves
dexamethasone suppression test
potent synthetic glucocorticoid
high doses suppress ATCH + cortisol (pit diseases)
ectopic ATCH not suppressed
adrenal diseases: low ACTH but high cortisol
low dose test also exists
Hyperaldosteronism
primary
overproduction of aldosterone
RAAS suppression - low plasma renin
HTN, hypernatraemia, hypokalaemia
dx = high aldosterone + low renin
causes
aldosterone producing adrenocortical neoplasm
80% of cases = adenoma (Conn's syndrome)
affects adults, midlife
F:M = 2:1
small, <2cm, difficult to detect
L>R
bright yellow
adrenocortical hyperplasia (bilat idiopathic)
glucocorticoid-suppressible hyperaldosteronism: rare, corrected when ACTH suppressed, mutation resulting in hybrid glomerulosa cells
tx: surgery (remove adenoma), aldosterone antagonist (spironolactone) to correct hyperplasia
secondary (extra-adrenal)
RAAS over activation - high renin
occurs in CHF, low renal perfusion (renal art stenosis), hypoalbuminuria (low plasma vol), pregnancy (oestrogen-induced, increases plasma renin substrate)
aldosterone
steroid hormone
acts on distal tubules + collecting ducts
Na + H2O retention, K secretion, increased circulating vol + BP (RAAS), increased perfusion of juxtaglomerular app