adrenal glands

Question 1

what are the 3 sections of the adrenal gland cortex

Answer 1

GFR -salt sugar sex (the deeper the sweeter)
zona glomelurosa - mineralocorticoids e.g aldosterone (kidney resorption)
zona fasiculata- glucocorticoids e.g cortisol (carb metabolism)
zona recticularis - androgens = sex hormones e.g testosterone or oestrogen

Question 2

what are corticosteroids and the different types

Answer 2

steroid hormones synthesised from cholesterol in the adrenal glands and gonads. they are lipid soluble meaning they bind intracellularly for gene trasncription

Question 3

examples of corticosteroids

Answer 3

glucocorticoids 
mineralcoricoids 
androgens 
oestrogens 
progestins

Question 4

explain how corticosteroids work

Answer 4

1. readily diffuse across plasma membrane
2. bind to glucocorticoid receptors
3. binding causes dissociation of chaperone protein e.g heat shock protein
4. receptor ligand complex translocates to nucleus
   (dimerisation with other receptors can occur as in they pair up)
5. receptors bind to transcription factors (regulates gene transcription) or glucocorticoid response element (results in GRE mediated effects.
   have androgen receptors for androgens and mineralocorticoid receptors for mineralcorticoids

Question 5

what is the carrier protein of aldosterone

Answer 5

serum albumin

Question 6

function of aldosterone

Answer 6

regulates plasma NA+, K+ and arterial blood pressure. regulation occurs in collecting duct of nephron and increases expression of Na+/K+ pump. this increases Na+ resorption and K+ excretion. water follows Na+ increasing blood vol and BP

Question 7

what happens during primary hyperaldosteronism

Answer 7

defect in adrenal cortex. e.g
bilateral idiopathic adrenal hyperplasia
aldosterone secreting adrenal adenoma (conns syndrome)
low renin levels meaning high aldosterone to renin ratio- this is the differentiating factor to secondary

Question 8

what happens during secondary hyperaldosteronism

Answer 8

due to over activity of RAAS
renin producing tumour e.g juxtaglomerular tumour
renal artery stenosis (looks like less blood)
high renin;aldosterone

Question 9

signs of hyperaldosteronism

Answer 9

high BP 
left ventricular hypertrophy 
store 
hypernatraemia (all being resorbed)
hypokalaemia (all being excreted)

Question 10

treatment of hyperaldosteronism

Answer 10

adenomas removed in surgery

spironolactone (mineralocorticoid receptor antagonist)

Question 11

when is glucocorticoid

Answer 11

released by ZF in response to ACTH

Question 12

carrier protein of glucocorticoid

Answer 12

transcortin

Question 13

actions of glucocorticoid

Answer 13

increased protein breakdown
increased lipolysis
increased gluconeogenesis
resistance to stress (more glucose, higher BP)
anti-inflammatory effects (inhibits macrophage activity/mast cell degeneration)
depression of immune system

Question 14

how is cortisol regulated

Answer 14

negative feedback inhibits ACTH release from anterior pituitary and CRH release inhibited from hypothalamus

Question 15

how does glucocorticoid act on metabolism

Answer 15

increased glucose= increases glycogen stores in liver
increased lypolysis from fat = resditribution of fat
break down of protein

Question 16

what is cushings syndrome and its signs and symptoms

Answer 16

excessive cortisol. plethoric moon-shaped face, buffalo hump and abdominal obesity (due to redistribution of fat)
purple striae - from weakening skin due to reduced proteolysis
weight gain, hyperglycaemia (excessive glucose) and hypertension (due to increased plasma glucose)

Question 17

exogenous and endogenous causes of cushings

Answer 17

external causes- due to prescribed glucocorticoids e.g steroid drugs
endogenous causes - due to benign pituitary adenoma secreting ACTH (cushings disease), excess cortisol produced by tumour (adrenal cushings) or non-piuitaryadrenal tumour producing