PHYS - Osmotic and Volume Regulation Flashcards
1
Q
EFFECT OF VOLUME ON ADH RELEASE
A
- Decrease in plasma volume
- Decrease P in circulation
- Decrease baroreceptor activity
- Stimulate ADH release
- Increase tubular permeability to H2O
- Increase H2O reabsorption
- Increase tubular permeability to H2O
- Stimulate ADH release
- Decrease baroreceptor activity
- Decrease P in circulation
2
Q
VOLUME STIMULUS VS OSMOTIC STIMULUS
A
- Osmotic stimulus → drink water → decrease Posm → decrease ADH → excrete H2O
- Volume stimulus → IV saline → increase EFV → decrease ADH → excrete H2O → increase Posm → increase ADH
- Regulate volume by regulating sodium reabsorption
3
Q
CONTROL OF EFV BY SODIUM
A
- Volume (stretch) receptors:
- Intrarenal – JG cells of afferent arteriole
- Venous stretch receptors
- Baroreceptors
- Regulate extracellular volume by regulating sodium reabsorption which then regulates water reabsorption
- The following mechanisms that act on Na+ retention in the kidney
- GFR
- Aldosterone
- Natriuretic hormone
- Peritubular pressure
- The following mechanisms that act on Na+ retention in the kidney
-
Glomerulotubular Balance (GTB) – ensures a constant percent of the filtered load of sodium gets reabsorbed
- Always about 67%, while the amount in the 67% will change based on sodium intake
- Increased Na+ intake → increased Posm
- First → shift of fluid from IFC compartment to EFC → increased water reabsorption → increased EFV
- → ADH release → increased EFV
- → thirst → consume water → increased EFV
4
Q
ALDOSTERONE
A
- Intercellular receptors in principle cells of the collecting duct
- Release stimulated by:
- Blood pressure/volume → Angiotensin II
- Hyperkalemia
- Affects protein synthesis
- Increases Na+ channels on apical (tubular) membrane
- Allows Na+ to rush in and depolarize membrane so that K is stimulated to diffuse into tubule
- Increases Na+/K+ ATPases on basal membrane (blood side)
- Enhances ATP synthesis
- Increases Na+ channels on apical (tubular) membrane
- Functions:
- Na+ reabsorption
- K+ excretion
- H+ excretion
5
Q
CS: CHANGES IN ALDOSTERONE LEVEL
A
-
Hypoaldosteronemia (adrenal insufficiency; Addison’s disease)
- Hyperkalemia
- Acidosis (K+ put into cells)
- Hypotension (salt wasting)
-
Hyperaldosteronemia
- Hypokalemia
- Alkalosis (K+ withdrawn from cells for pump function)
- Hypertension (without overt volume expansion)
- Primary – overstimulation of adrenal gland by a tumor
- Secondary – caused by RAS
6
Q
HORMONES AFFECTING SODIUM/H2O REABSORPTION
A
- Natriuresis – excretion of excess sodium in water
- Aldosterone - Na+ reabsorption in CD
- ADH - H2O reabsorption in CD
-
Angiotensin II
- Secreted in response to low GFR
- Stimulates adrenal gland to secrete aldosterone
- Direct increase in proximal Na+ reabsorption
-
ANP (Atrial natriuretic hormone)
- Binds membrane receptors in CD that GC*
- Prevents Na+ reabsorption
- Increases GFR in glomerulus (decreased Na+ reabsorption)
- Diminishes effects of renin, angiotensin II, and aldosterone
7
Q
CONGESTIVE HEART FAILURE
A
- CHF patients exhibit positive and increasing sodium balance
- Arterial baroreceptors function to maintain ECV (effective circulating volume)
- CHF → decreased CO → shift in blood volume to venous side → decreased P/V on arterial baroreceptors → renin/angiotensin II/aldosterone release → Na+ retention → increases Posm → increase ADH → H2O reabsorption
- With volume trapped in venous circulation → increased edema
- Treatment: diuretics to try to prevent edema
8
Q
CHRONIC KIDNEY DISEASE
A
- Progressive decline in GFR due to loss of nephrons
- However, sodium balance and plasma osmolarity are still maintained!
-
Sodium – overall filtered load decreases because of the decreased number of nephrons working to filtered the blood
- So, less plasma filtered per cycle through kidneys, and more sodium drawn out per cycle to maintain constant excretion rate
- Decreased filtered load
- Increased fractional excretion
- No change in excretion rate
-
Creatinine – since less plasma is being filtered, creatinine concentration builds up more quickly in plasma creating a steeper gradient for filtration
- More concentrated filtered load
- No change in excretion rate
9
Q
ERYTHROPOIETIN
A
- Kidneys function in regulation of RBC production
- Release erythropoietin in response to reduced tissue oxygenation
- 90% from kidney
- 10% from liver
- Erythropoietin stimulates HSCs in the bone marrow to produce proerythroblasts→ RBCs → increased tissue O2 → decreased erythropoietin release