Renal endocrinology

Question 1

How is ADH secreted?

Answer 1

1) ECF osmolarity is above 290mOsmoles
2) Aquaporin channels in hypothalamic neurones allow the water to exit cells
3) Osmoreceptors shrink and stretch sensitive channels open
4) Ca2+/Na+ enter the cell = AP
5) AP–>supraoptic and paraventricular neurones–>ADH IS RELEASED

Question 2

What does ADH do?

Answer 2

Released from the posterior pituitary
1-Increases the water reabsorption in DCT in the kidney
2-insertion of aquaporins into the walls of the DCT and collecting duct ( so water can re-enter blood )
3-increases thirst
(water retention , intake )

Question 3

osmolarity < 280mOsmoles , when plasma water levels are too high , what happens to ADH secretion

Answer 3

MORE CONCENTRATED SOLUTION INSIDE THE CELL (so water will move into the cell)

• aquaporins in hypo-thalamic neurones allow water to enter cells due to osmosis
• osmoreceptors expand causing stretch receptors to be deactivated = no Ca2+ and Na+ in cell= no AP = no ADH secreted = water is not reabsorbed in DCT so water is lost from the body= dilute urine !

Question 4

ADH and BP

Answer 4

1) Baroreceptors in the carotid sinus and aortic arch

2) Sense low bP = supraoptic nerves, paraventricular nerves are activated to release ADH

Question 5

what is aldosterone and what is its mode of action?

Answer 5

1) Mineralocorticoid releases by adrenal gland = Zona Glomerulosa
2) Released when plasma (K+) increases ACTH, ANG2, RENIN secretion increases, when BP decreases and pH decreases
3) Causes Na+ and water reabsorption via Na+/K+ ATPase expression In DCT and collecting ducts

Question 6

How does Aldosterone protect against hyperkalemia?

Answer 6

Increases K+/Na+ pump expression in DCT and Ducts, which causes Secretion of K+ into the lumen, causing loss of K+ to urine.
It can be reabsorbed down the line in DCT

Question 7

what is hyperaldosteronim

Answer 7

1- Primary =Conn’s disease (aldosterone adenoma )
2-Secondary: over activity of RAAS
Both lead to HT and hypokalemia

Question 8

what is HYPOaldosteronism
2 main types and causes
test to determine the cause ?

Answer 8

1-Primary adrenal insufficiency due to congenital adrenal hyperplasia, medication is ACE inhibitors and diuretics
Causes: hyperkalaemia, palpitations, muscle weakness, numbness and cardiac arrest
2- Secondary adrenal insufficiency = diseases of the pituitary or Hypothalamus

ACTH stimulation test for aldosterone can help determine the cause :
1-low aldosterone response =primary hypoaldosteronism , normal response = secondary hypoaldosteronsim

Question 9

Outline the RAAS recap

Answer 9

Afferent arteriole –>PCT with Macula Densa cell+ JG cells –>Efferent arteriole

1) BP decreases, or Na+ drops
2) Kidney detects low BP
3) RENIN= Angiotensinogen –>Ang 1 which goes to ANG2 –>Adrenal cortex –>Vasoconstrictor and Aldosterone is released Na+, K+ pump expression increases in DCT ( water is reabsorbed ), ADH is released from pituitary gland = increases thirst and water volume

Question 10

what is an Atrial Natriuretic peptide

Answer 10

1-released by atrial myocytes in response to atrial distension
2-ANP inhibits renin release
(reduced Ang 2, aldosterone, which will reduce BP)
= counterbalance of RAAS

Question 11

How can plasma osmolarity be controlled via thirst?

How do we know this is different from the ADH release?

Answer 11

We know it is different to the ADH release because:
1- Anticipate thirst
2-Thirst can be rapidly suppressed
3-Threshold is different to ADH