Other #2 Flashcards
Why do patients with CHF experience edema?
Patients with CHF will experience because they have decreased CO–> decreased ECV (think of it as decreased BP).
Our body will react by trying to compensate for the decreased ECV by completing 4 tasks:
- RAAS
- +Baroreceptors via sympathetic NS
- Increase ADH
- Increase renal fluid retention by altering Starling forces in the peritubular capillaries
- Increases rentention of Na+ and water will cause edema.
- Thus, our body is increasing the extracellular fluid volume without correcting for the ECV.
Changes in the amount of Na+ in our body is detected by measuring our effective circulatory volume (ECV) via cardiac and arterial baroreceptors.
- this causes changes in: _________________
- which will affect what?
Changes in Na+ is detected by measuring our ECV via baroreceptors.
This will then causes changes in [angiotensin II, aldosterone, SNS, ANP], which will alter Na+.
Changes in amount of body water is sensed by measureing _______ via ___________.
This causes changes in _________________, which will effect _____________.
Changes in our body water is measured by measuring our plasma osmolarity via osmoreceptors.
Osmoreceptors will then regulate ADH, which will then affect our urine osmolarity and thirst.
ECF volume and Na+ work hand in hand.
If we have an increase in total body Na+, how do we compensate?
We are going to have volume expansion.
ECF volume and Na+ work hand in hand.
If we have a decrease in Na+, what will happen to compensate?
Volume contraction.
How does our body compensate for decrease Na+ consumption
Volume contraction
Decreased Na+–> - osmoreceptors
- Decreased thirst–> decrease water consumption
- Decrease ADH–> decrease water reabsorption
Osmotic gradient is created and water will move from the ECF–> ICF
-concentrates ions in the plasma
–> HOMESTASIS
When the ECF volume increases, they kidneys excrete Na+ and H20.
What 4 mechanisms does this occur by?
1. RAAS system
- Angiotensin II –> + Na+ reabsorption along the nephron and cause the release of ADH
- Aldosterone –> + Na+ reabsorption in the DT and CD (and to some degree the thick ascending loop of Henle)
2. Renal sympathetic nerve activity
- Activatation of renal sympathetic nerves –> decrease NaCl excretion by decreasing GFR–> + renin secretion–> Na+ reabsorption
3. Natriuretic peptides (ANP, DNP, urodilatin)
4. ADH
What are the 3 major mechanisms for regulating renin?
-
Perfusion pressure
- Low perfusion in the afferent arterioles (as an low blood pressure) –> + renin secretion.
- High perfusion–> - renin secretion.
-
Sympathetic nerve activity
- Activation of the sympathetic nerve fibers in the afferent arterioles –> + renin secretion
-
NaCl delivery to the macula densa
- When NaCl is decreased–> + renin secretion
What is the primary action of ANP?
To decrease Na+ reabsorption in the distal parts of the nephron.
Hyponatremia will cause what?
Hyponatremia will cause water to go from the ECF–> ICF
Cells will swell and it will cause edema
If we lose water in the ECF, it will result in volume contraction.
What is the main way to regulate Na+ levels so that we can regulate our ECFV?
Aldosterone
Hyponatremia is defined osmolarities of
serum Na <135mOsm
serum osmolarity <280 mOsm
Where does ADH stimulate sodium chloride reabsorption?
Thick ascending loop of Henle, distal tubule, and collecting duct.
What is responsible for the negative feedback of ADH production?
ADH is short-lived, so when the baroreceptors or osmoreceptors are no longer firing, ADH stops being produced and it clears from the bloodstream.
Why might osmoreceptors not respond to high urea concentration in the blood?
Urea is an ineffective osmole, and does not affect AVP secretion
