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RB Y2 Endocrine - 4 Adrenal > Adrenal Glands - Hyperfunction > Flashcards

Adrenal Glands - Hyperfunction Flashcards

1
Q

what does the zona glomerulosa produce

A

aldosterone

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2
Q

what do the zone fasciculata and zona reticularis produce

A

fasciculata - cortisol

reticularis - androgens

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3
Q

what does the medulla produce

A

noradrenaline and adrenaline

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4
Q

what activates the RAAS system

A

decrease in blood pressure

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5
Q

what are the effects of aldosterone

A

increased cardiac collagen

cytokines and ROS synthesis

sodium retention

increased sympathetic outflow

altered endothelial function - increased pressor

increased blood pressure, LVH and atheroma

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6
Q

synthesis of steroids

A
  • They are synthesized from the same initial precursor cholesterol, and secreted on demand. They are lipid soluble (lipophilic) so when they are synthesized they are immediately capable of moving out of that cell (this is why they are secreted on demand).
  • bind to intracellular receptors, and bind to nuclear DNA affecting transcription
  • cholesterol - pregnenolone - progesterone (through the action of 3ßHSD)
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7
Q

what are the CNS actions of glucocorticoids

A

mood lability

euphoria/psychosis

decereased libido

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8
Q

what are the bone/connective tissue actions of glucocorticoids

A

accelerates osteoperosis by stimulating osteoclasts

decreased serum Ca, collagen formation and wound healing

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9
Q

what are the immunological actions of glucocorticoids

A

decreased:

  • capillary dilatation/permeability
  • leucocyte migration
  • macrophage activity
  • inflammatory cytokine production

suppress immune system to dampen pain response

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10
Q

what are the metabolic actions of glucocorticoids

A

carboydrate : inc blood sugar

lipid : inc lipolysis and central redistribution of it

inc proteolysis

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11
Q

what are the 3 main principles of use of glucocorticoids:

A

suppress inflammation

suppress immune system

replacement treatment

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12
Q

what are some causes of acquired adrenocortical hyperplasia

A

endogenous ACTH production: pituitary adenoma(Cushing’s disease) or ectopic ACTH (paraneoplastic syndrome - often SCLC)

bilateral adrenal enlargement as an inappropriate normal response

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13
Q

diffuse and nodular adrenocortical hyperplasia

A

diffuse - ACTH driven usually

nodular - usually ACTH independent

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14
Q

congenital adrenal hyperplasia syndromes

A

rare conditions associated with enzyme defects in the steroid pathway

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15
Q

most common form of CAH

A

the most common one is 21 hydroxylase deficiency (95% of cases), which affects one of the cytochrome p450 enzymes (p450c21)

results in reduced cortisol secretion, and this increases ACTH to maintain adequate cortisol, leading to adrenal hyperplasia

diversion of steroid pathway into androgenic pathway occurs

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16
Q

what is the result of the diversion of the steroid pathway into androgenic pathways in CAH

A
  • 17-hydroxyprogesterone, androstenedione and testosterone levels are increased, leading to virilization and precocious puberty
  • Aldosterone synthesis may be impaired with resultant salt wasting (low blood sodium concentration and dehydration).
  • Non-classically, there can be hyperandrogenaemia.
17
Q

diagnosis of CAH

A

basal (or stimulated with synACTHen test) 17 hydroxyprogesterone increased

increasingly suppported by genetic mutation analysis

basal ACTH levels raised

18
Q

define salt wasting

A

low blood sodium concentration and dehydration

19
Q

how can CAH present if severe

A
  • if severe, can present with sexual ambiguity or adrenal failure (collapse, hypotension and hypoglycaemia), sometimes with a salt losing state (hypotension and hyponatraemia)
  • eg Child may present with ambiguous genitalia, and then have severe vomiting, dehydration and weight loss
20
Q

clinical features of CAH

A

female: clitoral hypertrophy, urogenital abnormalities and labioscrotal fusion
male: can be unrecognised, poor weight gain, adrenal insufficiency (starts at around 2-3 weeks), biochemical pattern

precocious puberty

hirsutism

acne

oligomenorrhoea

infertility/sub-fertility

21
Q

what is the development of hirsutism before puberty suggestive of

A

CAH

22
Q

treatment principles of CAH in paediatrics

A

timely recognition

glucorticoid (and mineralocorticoid) replacement

surgical correction

achieve maximal growth potential

23
Q

treatment principles for adult physicians

A

control androgen excess

restore fertility

avoid steroid over replacement

24
Q

who do adrenocortical tumours tend to occur in

A

adults, although can occur in younger patients (especially those with Li-Fraumeni syndrome

25
Q

Li-Fraumeni syndrome

A

cancer predisposition syndrome caused by a germline mutation of p53 tumour suppressor gene

26
Q

what can carcinomas with necrosis cause

A

fever

  • pyrexia of unknown origin is a possible presentation
27
Q

adrenocortical adenoma

A

well circumscribed, encapsulated lesions

usually small and have a yellow/brown surface - preponderance of lipid laden cells

they are well differentiated with small nuclei

28
Q

adrenocortical carcinoma

A

rare

most of the lesions are clearly malignant at presentation with local spread (retroperitoneum/kidney) and/or metastases

29
Q

what are tumours secreting androgens, oestrogens or precursor steroids more likely to be

A

malignant

30
Q

what is the only definite criteria for malignancy

A

metastases

31
Q

what are features suggestive of adrenocortical carcinoma

A

large (>50g >20cm)

haemorrhage and necrosis

frequent mitoses, atypical mitoses

lack of clear cells (not well differentiated)

capsular/vascular invasion

assimilation of evidence

32
Q

Waterhouse Friderichen Sydnrome

A
  • Adrenal failure due to bleeding into adrenal gland
  • Commonly caused by severe bacterial infection, typically Neisseria Meningitidies

RB Y2 Endocrine - 4 Adrenal (5 decks)

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