adrenal steroids

Question 1

mineralocorticoid deficiency signs

aldosterone

Answer 1

hyponatraemia
*hyperkalaemia
hypotension
metabolic acidosis (increased H+)

Question 2

glucocorticoid deficiency
(cortisol)

Answer 2

hyponatraemia
*hypoglycaemia
hypotension

Question 3

likely combined glucocorticoid and mineralocorticoid deficiency

Answer 3

both

• hypoglycaemia
• hyperkalaemia

suggests primary adrenal problem

Question 4

mechanism of glucocorticoid hyponatraemia

Answer 4

• unable to excrete water load (reduced glomerular filtration rate)
• loss of cortisol inhibition of antidiuretic hormone
  (cortisol normally inhibits ADH release)
  will retain more water and dilute you

Question 5

mechanism of glucocorticoid hypoglycaemia

Answer 5

• reduced hepatic glucogenesis

Question 6

mechanism of glucocorticoid hypotension

Answer 6

• loss of cortisol effects on vascular tone

poor organ perfusion e.g. kidneys

Question 7

mechanism of mineralocorticoid hyponatramia

Answer 7

• urine Na+ loss with intravascular volume contraction and secondary ADH/vasopressin secretion
  - potent vasoconstrictor
  - more water retain from ADH not due to Na+ loss

Question 8

mechanism of mineralocorticoid hyperkalamia

Answer 8

• reduced renal K+ excretion

due to lack of aldosterone

Question 9

dehydration

Answer 9

loss of Na+ AND water

Question 10

mechanism of mineralocorticoid metabolic acidosis

Answer 10

• reduced renal H+ excretion (increased H+)

due to lack of aldosterone

Question 11

how is aldosterone made

Answer 11

lack of volume sensed at the juxta glomerular apparatus through Cl causing a release of renin

renin gets converted angiotensin 1
which then gets converted to angiotensin 2 via ACE

angiotensin 2 stimulates adrenal cortex to make aldosterone

(adrenal cortex also stimulates by ACTH and K+)

Question 12

action of aldosterone

Answer 12

increase Na+ and H20 reabsorption

increase intravascular volume

Question 13

causes of adrenal failure

Answer 13

primary = adrenal gland

secondary/tertiary
= pituitary/hypothalamus

Question 14

what does a lack of cortisol stimulate

Answer 14

release of more cortisol-releasing factor (CRF) from the hypothalamus and therefore ACTH from the pituitary

Question 15

how does a primary adrenal problem cause a tan

Answer 15

ACTH is a peptide product of POMC

POMC gets cleaved and produces melanocyte stimulating hormones MSH

therefore when you stimulate POMC to make more ATCH you also stimulate MSH
- increased levels of MSH in the bloodstream pigmentates your melanocytes

Question 16

what regulates ACTH

Answer 16

regulated by cortisol
- is independent of mineralocorticoid axis

increased POMC and ACTH occurs with a lack of feeback inhibition e.g. decreased cortisol in primary adrenal failure

Question 17

classically in primary adrenal insufficiency where is pigmentation seen?

Answer 17

more apparent in

• skin flexures
• nail beds
• mouth
• freckles
• old scars

Question 18

how to tell if an obesity is pathological

Answer 18

• sudden change in appearance over time (not gradual)
  pictures useful
• growth pattern (children) pathological cause = shorter

Question 19

glucocorticoid excess

Answer 19

in childhood = generalised obesity
causes profound growth failure

in adults = leads to truncal obesity
(obesity round the middle)

Question 20

features of glucocorticoid excess

Answer 20

• moon face
• thinning skin
• glowing skin
• easily bruised
• androgen excess e.g. amenorrhoea / irregular periods and hairy
• myopathy
• diabetes
• hypertension
• oesteoporosis

Question 21

cortisol binding and excess

Answer 21

cortisol binds to the mineralocorticoid receptor and the glucocortisol receptor with equal affinity

however cortisol is metabolised very quickly to cortisone and usually has no MC effect

IF kidney is overloaded with cortisol a mineralocorticoid effect can be observed
e.g. hypertension and hypokalaemia

Question 22

most common cause of glucocorticoid excess at a young age

Answer 22

pituitary tumour producing ACTH = cushings disease

Question 23

what do you get in you have partial loss of the glucocorticoid receptor

(note: receptor not hormone)

Answer 23

1. brain isnt going to see as much cortisol therefore is going to release more ATCH from the pituitary
2. ATCH makes adrenal glands bigger
3. more cortisol released
4. cortisol excess however will be seen as normal
5. too much cortisol will bind to MC receptor
   - mineralocorticoid excess –> hypokalaemia, hypertension

by products of cortisol is androgen

= glucocorticoid resistance

Question 24

secondary mineralocorticoid effects

Answer 24

• alkalosis
• hypokalaemia
• hypertension

hyperandrogenism
fatigue/tiredness (cortisol insensitivity)

this is a result of cortisol excess binding to MC receptors

Question 25

what do you get in you have a loss of function of the mineralocorticoid receptor

Answer 25

present as aldosterone deficiency

mineralocorticoid resistance

• high aldosterone and renin levels
• depleted extracellular fluid space = decreased ECF
• high serum K+ and low Na+ conc

Question 26

what happens when the ACTH receptor has a loss of function e.g. mutation

Answer 26

small nonfunctioning area of the adrenal cortex

severe cortisol deficiency from birth

• hypotension
• low Na+
• hypoglycaemia

Question 27

what does low cortisol levels lead to

Answer 27

high ACTH levels with secondary stimulation of the adrenal cortex, excess production of adrenal precursors (not cortisol but high levels of P4 and testosterone) and adrenal hyperplasia

Question 28

low K+ and high BP are signs of what?

Answer 28

aldosterone/mineralocorticoid excess