Steroid Abnormalities

Question 1

Mineralocorticoid deficiency (aldosterone) (4)

Answer 1

Hyponatraemia: Urine Na+ loss with water, as well as secondary ADH which retiains the water but salt still lost. Dilute
Hyperkalaemia*: Reduced renal K+ excretion
Hypotension
Metabolic acidosis: Reduced renal H+ secretion

Question 2

Glucocorticoid deficiency (cortisol) (3)

Answer 2

Hyponatraemia: Unable to excrete water load due to loss of vascular tone and loss of cortisol inhibiton of ADH- WATER RETENTION
Hypoglycaemia*: Reduced hepatic gluconeogensesis
Hypotension: loss of cortisols effects on vascular tone

Question 3

Mechanism of mineralocorticoid action

Answer 3

JuxtaG apparatus- Renin- Angiotensin 1-ACE- Angiotensin 2- Adrenal Cortex (as well as K+ and a bit of ACTH)- Zona glomerulosa- Aldosterone- increased Na+ and water retained and K+ excretion. Increased volume turn of renin

Question 4

Two causes of adrenal failure

Answer 4

Primary: GLAND
Secondary: Pituitary, hypothalamus

Question 5

Cortisol feeback loop

Answer 5

Hypothalamus- CRF - Pituitary (ANT) - Adrenal cortex to release cortisol.
Cortisol has negative feedback on hypothalamus and pituitary

Question 6

Why does primary adrenal failure cause a tan?

Note skin pigmentation increased in skin folds, scars, freckles

Answer 6

ACTH is a product of POMC. 3 MSH are made of cleavage of these POMC’s
1 MSH in ACTH also
Lack of cortisol inhibiton means increased POMC, meaning ACTH, meaning increased MSH

Question 7

Simple versus generalised obesity

Appearance over time: ____ obesity apparent by 3-4, and worsens with age; An excess of GC’s leads to _____ obesity. In adults, truncal obesity
Growth pattern: ____ obesity drives growth, taller than expected, then at puberty get to parents height. GC excess leads to _____ ______.
Other pathological causes

____ ____ CHILD has underlying cause unless proven otherwise

Answer 7

Appearance over time: Simple obesity apparent by 3-4, and worsens with age; An excess of GC’s leads to general obesity. In adults, truncal obesity
Growth pattern: Simple obesity drives growth, taller than expected, then at puberty get to parents height. GC excess leads to growth stunting.
Other pathological causes

SHORT FAT CHILD has underlying cause unless proven otherwise

Question 8

Other features of GC excess (e.g Cushings syndrome, pituitary abnormality)

Answer 8

Moon face
Skin thinning (bruising etc)
Androgen excess: hirsutism, amenorrhea
Myopathy
Diabetes mellitus
Hypertension
Osteoporosis

Question 9

What can be said about cortisol and its affinity for the MC receptor?

Answer 9

Same affinity but rapidly broken down (11B hydroxysteroid dehydrogenase type 2).
In excess MC effects can start to be seen, like hypertension (apparent increased aldosterone)

Question 10

What happen with partial loss of GC receptor?

Answer 10

Increased cortisol (feedback loop)
Secondary mineralocorticoid receptor effects such as hypokalaemia, alkalosis, hypertension.
Hyperandrogenism; fatigue

Question 11

What happens with loss of MC receptor

Answer 11

pseudohypoaldosteronism
High aldosterone
Hyperkalaemia, hyponatraemia, hypotensive

Question 12

What happens with ACTH receptor loss of function

Answer 12

No cortisol, hypotension, low Na+, hypoglycaemia

Question 13

Congenital adrenal hyperplasia

Answer 13

Defect in enzyme involved in cortisol synthesis. (usually 21 hydroxylase defect) low cortisol
leading to high levels of ACTH, meaning adrenal hyperplasia making a lot of adrenal percursors (17 OH progesterone and P4). These are converted to testosterone, causing virilisation

Question 14

Management of CAH

Answer 14

GC therapy to suppress ACTH release

Inhibit central precocious puberty

Question 15

Causes of Cushings

Answer 15

Adrenal tumour
ACTH producing pituitary tumour
Ectopic ACTH syndrome

Exogenous

Question 16

Addisons disease

Answer 16

Hypocortisolism, insufficiency of adrenal glands typically.

Question 17

NB all steroid creams

Answer 17

Go straight into blood stream, can cause exogenous cushings