Na handling Flashcards
What is EABV?↓↑→
which limb detects the changes in EABV?
effective arterial blood vol
- volume of blood that is detected by volume sensors, located on arterial side of circulation
- afferent limb has volume receptors for EABV
What is the efferent limb responsible for regulating?
regulates the rate of Na+ excretion by the kidney
note the afferent limb is responsible for volume sensing
4 categories of volume sensing in the afferent limb?
- low P baroreceptors
- high P baroreceptors
- intrarenal baroreceptors
- hepatic and CNS sensors
Low P baroreceptors include
- cardiac atria receptors
- LV receptors
- Pulm vascular bed receptors
Which receptors are located on the arterial side of the circulation and protect the body against volume contraction and expansion?
the high P recetors:
Carotid sinus body @ bifurcation
aortic body @ arch
*note that the low P receptors are located on the venous side
What happens if EABV is low?
If it is low → volume contraction state → signals the brain → ↑ renal SNS
*if really severe volume contraction, NE is released
Tubuloglomerular feedback
phenomenon where ↑ NaCl to the macula densa, ↑s afferent arteriolar tone and corrects GFR
Glomerulo-tubular balance
fundamental property:
- changes in GFR causes proportional (fractional) change in the rate of PROXIMAL tubular sodium reabsorption
What effects do NO, PGE2, PGI2 have on GFR?
It induces vasodilation of aff a → increases GFR (thus maintaining it - keeps it up)
*note that AGII vasoconstricts the efferent arterial to also increase GFR
What effects do NSAIDS, ACE-I, ARBs have on GFR? how
NSAIDS decrease GFR by inhibiting the vasodilatory effects of PG
ACE-I and ARBs inhibit AGII vasoconstriction effects on Eff arterioles
During states of volume contraction, which hormones act to induce antinatriuresis?
antinatriuresis (increase Na reabsorption)
- Ag II
- aldosterone
- catecholamines
- vasopressin
During states of volume overload, which hormones act to induce natriuresis?
natriuresis (pee more)
- natriuretic peptide
- PGs
- Bradykinin
- Dopamin
activation of the renal SNS induces what: natriuresis or antinatriuresis?
antinatriuresis
SNS is usually stim in state of volume contraction
(stim release of renin → increases AGII → antinatriuresis)
3 ways that Na is reabsorbed into the cell, in the Distal tubule
- Na channels
- NaCl cotranporters
- Na/H antiporter
2 ways that Na is reabsorbed, into the cell, in the thick ascending loop of henle
- NaK2Cl
2. Na/H antiporter
name which receptor these drugs inhibit:
- Loop diuretics
- thiazide
- amilioride
- NaK2Cl
- Na/Cl cotransporter
- Na channel
two types of cells in cortical collecting duct and their purpose
- principal cells:
- exchanges a ton of shiz (Na, K, Cl, HCo3) - intercalated cells
- H+ secretion
- HCO3- secretion
First clinical signs of mild volume contraction
- orthostatic HTN
2. tachycardia
What happens to BUN levels during states of volume contraction
increased BUN
volume contraction → kidney avidly reabsorbs Na+ in prox tubule → urea follows Na+ → ↑ BUN
Saline expands ___________ volume acutely.
ECF: electrolytes move freely between intravascular and interstitial spaces
How does congestive HF result in ECF volume expansion?
increased venous P → increases capillary hydrostatic P → Fluid move to interstitial compartment
How does nephrotic syndrome result in ECF volume expansion?
urinary protein loss → decrease capillary oncotic P → decrease vessel ability to retain water → water moves into interstitial comp
How does cirrhosis result in ECF volume expansion?
- hypoalbuminemia: decrease in capillary oncotic P
2. Increased splanchnic vasodilation (seen in cirrhosis): increase in capillary hydrostatic P
Diuretic abuse in pts
excessive use of diuretics can worsen kidney fxn by intravascular vol depletion
