Lecture 6 - Control of Blood Volume & Osmolality

Question 1

The RAAS is stimulated in response to low BP, what 3 things stimulate renin production & release from the JGA?

Answer 1

1) Increased sympathetic innervation
2) Decrease in afferent arteriole wall tension
3) Decreased NaCl delivery at the macula densa

Question 2

What are the effects of angiotensin ll?

Answer 2

1) Causes vasoconstriction of the efferent arterioles in glomerulus
2) Stimulates aldosterone release from zona glomerulosa, which increases Na+ reabsorption in DCT, releases ADH & stimulates thirst

Question 3

What are the renal responses to increased blood pressure?

Answer 3

1) Release of ANP from atrial cells in response to increased ECF volume

• Inhibits Na/K ATPase of CD’s and DCT to reduce Na+ reabsorption
• Vasodilation of afferent arteriole increasing GFR
• Inhibits aldosterone, ADH & renin release

2) Increase in hydrostatic pressure of peritubular capillaries leads to increased Na+ excretion (pressure natriuresis) and increased water excretion (pressure diuresis)

Question 4

How do the response of the kidneys in congestive cardiac failure make the situation worse?

How is this managed clinically?

Answer 4

• CCF is when heart muscle pump cannot cope with workload, CO falls and fails to perfuse tissues.
• Renal hypo perfusion sensed by kidneys as hypovolaemia, resulting in compensation by retaining NaCl & H2O to increase circulating volume
• This increases pulmonary venous pressure, causes transudation from the capillaries into the lungs & pulmonary oedema.
• Management is reducing fluid load by diuretics, ACE inhibitors, nitrates etc

Question 5

What is hypervolaemia and how is it typically caused?

Answer 5

• Fluid overload, excess of total body Na & H2O leading to expansion of ECF
• Typically due to kidney retention of Na & H2O, CCF, excessive Na/H2O intake, hyperaldosteronism

Question 6

What is hypovolaemic shock & how is it caused?

Answer 6

• A lack of circulating volume from blood loss, burns, diarrhoea etc. Vital organs are inadequately perfused, hypoxic state causes anaerobic metabolism causing metabolites to build up. Vasodilation occurs in vital organs to maintain blood supply.

Question 7

How are the kidneys affected by hypovolaemic shock?

How is hypovolaemic shock treated?

Answer 7

• They’re inadequately perfused due to diversion of blood to vital organs, leads to acute tubular necrosis
• Extra fluid replacement to restore ECF volume, if blood flow to kidneys not restored, tissue anoxia & necrosis occurs

Question 8

How can the kidney itself caused secondary hypertension?

Answer 8

• Impaired Na/H2O excretion increases blood volume

- Renal artery stenosis causes reduced perfusion of the kidney and therefore excessive activation of RAAS

Question 9

What is the response to increased plasma osmolality ?

Answer 9

• Osmoreceptors in hypothalamus sense increase in hypothalamus, which trigger ADH release and increase in thirst.
• ADH binds to V2 receptors on BL of CD cells, causing fusion of AQP2 channels on luminal membrane and increased reabsorption of water
• Thirst stimulated to increase intake of water

Question 10

What is central & nephrogenic diabetes insipidus?

Answer 10

Central = impaired ADH secretion/synthesis by hypothalamus, i.e.: due to brain injury, tumour, aneurysm, meningitis etc. Large quantities of dilute urine produced. Treated with desmopressin.

Nephrogenic = Acquired insensitivity to ADH, large amounts of dilute urine produced. Treated with low salt, low protein diet.

Question 11

What is syndrome of inappropriate ADH secretion (SiADH)?

Answer 11

• Excessive release of ADH from PP or another source, causing dilutional hyponatreamia, increased total body fluid, very concentrated urine.
• Diagnosis made is hyponatraemic patients in absence of hypovolaemia, oedema, endocrine dysfunction etc.