regulation of body fluid volume Flashcards

1
Q

What is effective circulating volume?

A
  • The Effective Circulating Volume (ECV) refers to the portion of extracellular fluid that is in the arterial circulation and effectively perfusing tissues. It varies with ECF volume and total body sodium stores. ECV is maintained by varying vascular resistance, cardiac output, and renal sodium and water excretion.
    ○ Usually 700ml in atrial system in 70kg man
    ○ Effectively perfusing tissues
    ○ Body can’t measure total blood in all compartments but can measure the effective perfusing tissue therefore, the body directly controls the volume of the intervascular tissue and influences volumed on other compartments
    ○ Not all of the blood sometimes will go into the kidneys
    ○ Volume of blood perfusing organs/tissues can change without changes in the blood volume
    § Durning heart failure some blood stays behind in the heart as the heart can’t contract as strongly-decreased cardiac output
    § liver cirrhosis is blood will stay in the liver-increased splanchnic vasodilation
    • High volume=high pressure and low volume=low pressure
    • If the volume of the blood/blood pressure changes the kidneys will compensate by changing the Na+ concertation in the blood
      ○ if high blood pressure more Na+ will be secreted into the urine which will cause the osmolality to decreased and less aquaporins to be inserted into the DCT and collecting duct this means that less water will be reabsorbed/more urine will be produced
      ○ if low blood pressure less Na+ will be secreted into the urine which will cause the osmolality to increase and more aquaporins to be inserted into the DCT and collecting duct this means that more water will be reabsorbed/less urine will be produced
    • Osmolality problems fixed by ADH but pressure problems fixed by Na+
      ○ If you get a question about volume or pressure of the blood changing then always think about kidneys changing Na+ to change the plasma volume
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2
Q

How is the effective circulating volume (ECV) detected/What are the components of the juxtaglomerular apparatus?

A
  • The juxtaglomerular apparatus (JGA) is a group of cells in the kidney that regulates blood flow, filtration rate, and sodium chloride balance
    • Baroreceptors
      ○ Detects changes in pressure (stretch) perfusing though them
      ○ Systematic arterial barrow receptors found in the carotid artery sinus and the arch of the aorta
      ○ Kidneys have their own pressure receptors in their Afferent Arterioles
      § Every nephron can monitor fluid volume/blood pressure
      § In the afferent arteriole the smooth muscle is very close to the glomerulus- modified cells to become baroreceptors-juxtaglomerular cells (granular cells)
      § juxtaglomerular cells release renin when the blood pressure drops
    • Chemoreceptors
      ○ Detects changes in chemicals
      ○ Found inside the DCT (DCT comes very close to the glomerulus =juxtaglomerular apparatus)
      ○ Inside the DCT there are tubular cells that have been modified into chemoreceptors-macula dense cells
      § Also cause the release of renin
      *
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3
Q

What the Renin-Angiotensin-Aldosterone System (RAAS)?

A
  1. Less blood goes into Afferent arteriole if there is a low blood pressure so pressure in the arteriole drops and is detected by Barrow receptors/Juxtaglomerular cells
    1. Juxtaglomerular cells release renin into the glomerulus
      ○ renin can’t be filter out as it is too large
      ○ Renin will be circulating in the blood
    2. GFR will drop if the blood pressure drops
      ○ Filtrate will go slowly down the PCT as there is a lower GFR
      ○ More sodium is reabsorbed at the PCT and is put back into the blood
    3. Chemoreceptors in the DCT detects lower Na+ concertation in filtrate
    4. Chemoreceptors send impulse to Barrow-receptors in Afferent Arterioles to release renin into the glomerulus
    5. Angiotensinogen is always present in the blood but doesn’t do anything until renin is released
      ○ Angiotensinogen is a globular protein
      ○ Produced by the liver
    6. Angiotensinogen converted to angiotensin I by renin
    7. angiotensin I converted to angiotensin II by angiotensin converting enzyme (which is produced by the kidneys)
      i. Angiotensin II will go to hypothalamus to stimulate thirst receptors so you drink more water to increase blood volume and therefore increase hydrostic pressure
      ii. Causes aldosterone to be released from adrenal glands to get more Na+ reabsorbed in the whole nephron
      ▪ Aldosterone goes to the collecting duct and causes more Na+ channels to embedded in the collecting duct so more. This makes the collecting duct (which WAS impermeable to Na+ permeable to Na+) so Na+ is reabsorbed into the blood
      ▪ This will increase the blood osmolality and cause water to be reabsorbed
      ▪ Gets more water to follow to sodium and go into the blood
      ▪ Biggest factor in how kidneys handle Na+ to raise blood pressure
      iii. Causes ADH to increase aquaporins and increase volume of the blood
      ▪ No change to osmolality when you have a haemorrhage/blood is lost as water and osmolality are both lost
      ▪ No change in osmolality usually wouldn’t effect ADH but aldosterone will cause ADH to be released from the posterior pituitary gland
      ▪ ADH will cause more aquaporins to be embedded in the collecting duct therefore reabsorbing more water and increasing the blood volume/pressure
      ▪ Doesn’t affect the amount of solutes excreted
      iv. Will raise pressure in glomerulus by contracting efferent arteriole to raise hydrostatic pressures and aloe kidneys to keep working as waste products need to be removed
      ▪ Contraction of the efferent arteriole will cause the hydrostic pressure in the kidneys to increase/normal so GFR is the same and body can still remove waste
      v. Will also cause vasoconstriction to raise blood pressure
      ▪ Decreases the size of the lumen of blood vessels so blood pressure increases
      vi. Reduced the excretion of NaCl by stimulating its reabsorption in the LoH, DCT and collecting duct
      ○ Removal of the adrenal glands will cause death in 2 weeks as Na+ isn’t being reabsorbed and circulatory collapse occurs
      *
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4
Q

Talk about the inhibition of the Renin-Angiotensin-Aldosterone System (RAAS).

A
  • Blood pressure is higher than normal e.g.
    ○ due to intake of (1L) of isotonic solution
    ○ Too much salt in the blood so H2O is retained
    • The higher volume causes stretching of the atria of the heart
    • Atria detects this stretch and relaces Atrial Natriuretic peptide (APN)
    • APN is secreted and stored by cardiac myocytes
      ○ Protein that effects the Na+ in the urine and is released from the atriums
    • Atrial Natriuretic peptide causes the Renin-Angiotensin-Aldosterone System to turn off so less water is reabsorbed
    • Drugs
      ○ Renin inhibition- Aliskiren
      ○ Angiotensin converting enzyme inhibitor- captopril, enalapril, ramipril
      ○ Ang II receptor antagonist/blockers-candesartan, irbesartan
      ○ Aldosterone receptor antagonist- spironolactone
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