Adrenal Gland Pathology Flashcards

1
Q

how much do adrenal glands weigh

A

4-5 grams each

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where do the adrenal glands sit

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the adrenal glands composed of

A

outer cortex and inner medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what 3 zones are is the adrenal cortex split up into

A

zona glomerulosa, zona fasciculata and zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is produced and secreted in the zona glomerulosa

A

mineralocorticoids and aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is produced and secreted in the zona fasciculata

A

glucocorticoids and cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is produced in the zona reticularis

A

sex steroids and glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is the adrenal medulla

A

central core of adrenal (extension of nervous system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what innervates the adrenal medulla

A

pre-synaptic fibres from sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what do neuroendocrine (chromaffin) cells secrete

A

catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes adrenocortical hyperfunction

A

hyperplasia, adenoma, carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what causes adrenocortical hypofunction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

who gets adrenocortical tumours

A

usually adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

25
are adrenocortical tumours usually functional or non-functional
functional (virtualising tumours usually malignant)
26
are adrenocortical adenomas or carcinomas more likely to be function
adrenocortical carcinomas
27
what is associated with the spread of adrenocortical carcinomas
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
what is the 5 year survival rate and mortality of adrenocarcinomas
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
what is the only criteria to distinguish between benign and malignant tumours
metastasis
30
what are some features to suggest carcinoma over adenoma
large size (>50g often >20cm in max dimension), haemorrhage and necrosis, frequent mitoses, atypical mitoses, lack of clear cells, capsular or. vascular invasion
31
what causes primary. hyperaldosteronism
Conn's syndrome, usually 60% associated with diffuse or nodular hyperplasia of both adrenal glands, adenoma, rarely carcinoma, glucocorticoid remediable
32
what causes secondary hyperaldisteronism
increased renin, decreased renal perfusion, hypovolaemia, pregnancy
33
what causes hypercortisolism
cushings,