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Endocrine > Adrenal Gland Pathology > Flashcards

Adrenal Gland Pathology Flashcards

1
Q

how much do adrenal glands weigh

A

4-5 grams each

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2
Q

where do the adrenal glands sit

A

superior and medial to upper pole of kidneys (embedded in perineal fat)

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3
Q

what are the adrenal glands composed of

A

outer cortex and inner medulla

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4
Q

what 3 zones are is the adrenal cortex split up into

A

zona glomerulosa, zona fasciculata and zona reticularis

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5
Q

what is produced and secreted in the zona glomerulosa

A

mineralocorticoids and aldosterone

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6
Q

what is produced and secreted in the zona fasciculata

A

glucocorticoids and cortisol

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7
Q

what is produced in the zona reticularis

A

sex steroids and glucocorticoids

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8
Q

where is the adrenal medulla

A

central core of adrenal (extension of nervous system)

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9
Q

what innervates the adrenal medulla

A

pre-synaptic fibres from sympathetic nervous system

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10
Q

what do neuroendocrine (chromaffin) cells secrete

A

catecholamines

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11
Q

what causes adrenocortical hyperfunction

A

hyperplasia, adenoma, carcinoma

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12
Q

what causes adrenocortical hypofunction

A

acute: Waterhouse-Friderichsen syndrome
chronic: Addison’s disease

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13
Q

what is the sequence of events leading to congenital adrenocortical hyperplasia

A

group of autosomal recessive disorders, deficiency/lack of enzyme required for steroid biosynthesis, altered biosynthesis leads to increased androgen production (masculinisation or precocious puberty), reduced cortisol stimulated ACTH release and cortical hyperplasia (10-15X normal. weight)

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14
Q

what can cause acquired adrenocortical hyperplasia

A

endogenous ACTH production (pituitary adenoma (cushings disease) or ectopic ACTH secretion (paraneoplastic syndrome from small cell lung cancer)), bilateral adrenal enlargement (up to 30g), diffuse or nodular (diffuse-ACTH driven and nodular-usually ACTH independent)

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15
Q

who gets adrenocortical tumours

A

usually adults

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16
Q

what syndrome is associated with younger patients with adrenocortical tumours

A

Li-Fraumeni syndrome (germline mutation of p53 gene)

one feature of this syndrome is an association with adrenocortical tumours

17
Q

how does an adrenocorical tumour present

A

incidental, hormonal effects if functional, mass lesion (has to be quite big-can undergo central necrosis), carcinomas with necrosis can cause fever (fever with no known cause is. sign of malignancy)

18
Q

are adrenocortical adenomas benign or malignant

A

benign

19
Q

how are adrenocortical adenomas usually found

A

incidentally

20
Q

what is characteristic of adrenocortical adenomas

A

well circumscribed, encapsulated lesions, well differentiated, small nuclei, rare, mitoses, yellow

21
Q

how big are adrenocortical adenomas

A

2-3cm (won’t present as mass lesion)

22
Q

what cells are adrenocortical adenomas composed of

A

cells resembling adrenocortical cells

23
Q

are adrenocortical adenomas usually functional or non-functional

A

non-functional (cause no problems)

24
Q

are adrenocortical carcinomas common or rare

A

rare

25
Q

are adrenocortical tumours usually functional or non-functional

A

functional (virtualising tumours usually malignant)

26
Q

are adrenocortical adenomas or carcinomas more likely to be function

A

adrenocortical carcinomas

27
Q

what is associated with the spread of adrenocortical carcinomas

A

local invasions (retroperitoneum, kidney), metastasis (vascular: liver, lung and bone (usually first sign of metastatic disease)), peritoneum and pleura and regional lymph nodes (tends to be vascular over lymphatic though)

28
Q

what is the 5 year survival rate and mortality of adrenocarcinomas

A

20-35% at 5 years, 50% dead in 2 years (could be due to arising in relatively silent site, by the time it is found not a lot that can be done)

29
Q

what is the only criteria to distinguish between benign and malignant tumours

A

metastasis

30
Q

what are some features to suggest carcinoma over adenoma

A

large size (>50g often >20cm in max dimension), haemorrhage and necrosis, frequent mitoses, atypical mitoses, lack of clear cells, capsular or. vascular invasion

31
Q

what causes primary. hyperaldosteronism

A

Conn’s syndrome, usually 60% associated with diffuse or nodular hyperplasia of both adrenal glands, adenoma, rarely carcinoma, glucocorticoid remediable

32
Q

what causes secondary hyperaldisteronism

A

increased renin, decreased renal perfusion, hypovolaemia, pregnancy

33
Q

what causes hypercortisolism

A

cushings,

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