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REGUB: Adrenal & Parathyroid Pathology (ii) (Adrenocortical neoplasms,…
REGUB: Adrenal & Parathyroid Pathology (ii)
Adrenogenital syndromes
disorders of sexual differentiation
primary gonadal disorders
primary adrenal disorders
2 compounds secreted by adrenal cortex
dehydroepiandrosterone
androstenedione
both converted to testosterone in peripheral tissues
androgen adrenocortical neoplasm: carc > adenoma
congenital adrenal hyperplasia
group of AR disorders
enzyme involved in synthesis if cortisol deficiency - ACTH increase - increased androgen production
90% 21-hydroxylase (no aldosterone or cortisol) - also hyponatraemia, hyperkalaemia, acidosis, hypotension, CV collapse, death
virilisation (development of male characterisitcs in a female or precociously in a boy)
Adrenal hypofunction (insufficiency)
primary adrenal disease
acute (adrenal crisis)
emergency
causes
rapid withdrawal from exogenous steroids, or failure to increase dose when patient under stress
Addison's precipitated by stress (infections, trauma, surgery) which requires increases steroid output
massive adrenal haemorrhage
anticoag tx
DIC - purpura on skin
bacteraemia (Waterhouse-Friderichsen - usually N meningitides, also can be pseudomonas, pneumococcus, staph, H influenzae, affects children more, clinical course abrupt + devastating, tx with antibiotics, early recognition NB)
intractable vomiting, abdo pain, hypotension, coma, vasc collapse
haemorrhagic necrosis
can lead to shock
Chronic (Addison's disease)
progressive destruction of cortex
90% must be destroyed for clinical manifestations to appear
Causes
60-70% due to AI adrenalitis
50% a/w other AI (e.g. Hasimoto's. pernicious anaemia, T1DM, hypoparathyroidism)
increased with HLA-B8 + DR3 (histocompatibility antigens)
infections (esp TB)
met carc (usually seeding of lung/breast)
progressive weakness, fatiguability, GI symptoms (anorexia, N+V, weightloss), hyperpigmentation (increased ACTH stims melanocyte), hyperkal, hyponat, hypotension, hypoglyc
stresses can induce adrenal crisis
secondary
ACTH deficiency (pit)
mets
infection
infarct
radiation
ALDOSTERONE STILL NORMAL (only cortisol + androgens low)
exogenous admin of ACTH results in prompt rise in cortisol
Adrenocortical neoplasms
F>M
age 30-50
functional neoplasms may be responsible for any form of hyperadrenalism
if functioning: suppression of endogenous ACTH - atrophy of adjacent cortex + contralat gland
adenomas
most clinically silent (incidental find)
well-circumscribed, encapsulated, <5cm, <30g
appear yellow due to lipid content in tumour cells
haemorrhage, cystic degeneration, or calcification
microscopically cells are similar to cortex but with mild pleomorphism
tx = surgical excision
carcinomas
rare
functional > non-functional
virilism + hyperadrenalism
usually >20cm when dxed
macro: poorly demarcated, necrosis, haemorrhage, cystic change
micro: range from well-differentiated cells to undifferentiated carc
invade adrenal vein, vena cava, lymphatics
mets to regional nodes, lungs or other viscera (bone mets uncommon
median survival = 2 yrs
myelolipoma
benign
incidental find
fat + haematopoietic cells
may reach massive proportions
Adrenal medulla
composed of neuroendocrine cells (chromaffin cells - produce catechols) + sustentacular cells (supporting cells)
symp NS stims chromaffin cells - increase rate + force of myocardial contractions + vasoconstriction
diseases
pheochromocytoma (neoplasms of chromaffin cells)
neuronal neoplasms
neuroblastoma
sporadic but familial cases do occur
most common extracranial tumour of childhood
ganglion cell tumours
Parathyroid glands
derived from pharyngeal pouches
not just in thyroid, can be found anywhere in ant mediastinum
10% of people have only 2/3
35-40mg
cells
parathyroid chief cells
oxyphil cells in smaller prop
PTH
osteolysis
bone resorption
renal tubular reabsorption of Ca (active vit D needed)
PO4 excreted