Renal II Flashcards
difference between osmolarity and osmolality?
R= osmol/L L= osmol/kg
what is antidiuresis?
normal land-dweller state: when you have high ADH in the blood, urine excretion is low, high reabsorption of urea
what contributes to the hyperosmotic gradient from cortex to medulla?
urea- 50%- 600 osmol
Na- 25%- 300 osmol
Cl- 25%- 300 osmol
3 mechanisms that generate hyperosmotic gradient from from cotex to medulla?
- countercurrent multiplier- permeability differences for Na and H20
- urea cycle- leaking out in collecting duct & only participating in right loop
- countercurrent exchanger- slow vasa recta flow (permeable to everything) allows time for Na to move in and H20 to move out
5 requirements for hyperosmolarity
1) long loops of Henle
2) blood & urine flowing in opposite direction
3) active salt pumping (in basolateral membrane of cells near TAL/DT/CD)
4) differential permeabilities
5) destruction takes days to re-establish
equation for osmolar clearance (Cosm)
Cosm= V * Uosm/Posm
what is Ch20? what is -Ch20 also called? what is the equation for Ch20?
Ch20= the amount of pure water kidney adds to urine -Ch20= TcH20
Ch20= V-Cosm
do alterations in Na change the volume or Na concentration of the ECF?
only the volume!!
what is the ECV?
effective circulating volume- the portion of the ECF that is effectively perfusing the tissues (normally direction proportional to ECF)
what are the 4 ways of regulating renal salt excretion via afferent sensors?
a- venous (increased atrial stretch, increased ANP, natriuresis)
b- arterial (increased barros, decreased symp, decreased ADH)
c- hepatic sensors (increased liver p, decreased symp)
d- CNS sensors (increased Na in CSF, decreased symp)
what is natriuresis?
increased sodium secretion in urine, followed by water
what is the sympathetic pathway
increased sympathetics decreases GFR by constricting afferent arteriole, which increases renin (RAAS) and increases Na reabsorption
what are the affects of angiotensin II and aldosterone?
angiotensin II- Na is reabsorbed proximally, causes secretion of ADH
aldosterone- increases NA reabsorption in TAL, DT, CD
how do ANP, BNP, and urodilatin work?
decrease aldosterone, decrease renin (decreases Na reabsorption), (decrease sympathetics- increase GFR- increase Na in tube- increase Na excretion)
what are the 3 things that stimulate renin secretion?
1) perfusion pressure sensed by baroreceptors in afferent arteriole
2) sympathetic nerves that innervate afferent arterioles
2) tubuloglomerular feedback senses decreased NaCl in macula densa
when is ANP released from atria?
1) increase in extracellular fluid volume
2) increase in arterial pressure (increase in LV pressure)
3) increase in venous pressure (increase in right atrial pressure)
what does reabsorption depend on in 3 parts of kidney?
1- proximal- filtered load
2- TAL- Na delivery rate
3- DT/CD- Na load remaining
during euvolemia, you have a _______; what percent of Na is filered?
net zero Na balance
-99% is filtered
what happens to GFR during volume expansion?
GFR increases, decrease reabsorption in proximal tubule and collecting duct
- see decrease sympathetics, increased urodilatin, increased ANP and BNP
what happens during edema? how can it be fixed?
- see decrease in ECV and plasma volumes
- fixed by giving diuretics to decrease Pc and increase PIc
what are 3 things that cause K+ release from the cell?
1) epinephrine acting on alpha receptors
2) cell lysis (burns, surgery)
3) hyperosmolarity
what are 5 things that cause K+ uptake by the cell?
1) epinephrine activating B2 receptors, especially during exercise
2) increased extracellular K+ stimulating the Na/K ATPase
3) insulin (especially following a meal)
4) aldosterone
5) hyposmolarity
what percent of K+ in kidneys is reabsorbed? what percent is excreted?
85-95% is reabsorbed (decreases with more in diet)
15-80% is excreted (increased with more in diet)
what 3 factors regulate K+ secretion in the DT & collecting duct
1) Na-K atp pump
2) cell-lumen -40 electrochemical gradient
3) K+ permeability of apical membrane
5 factors altering K+ secretion
1) hormones (aldosterone, GCs ADH)
2) tubular fluid flow
3) dietary intake
4) metabolic acidosis
5) diuretics
3 hormones that control distribution of Ca2+ between bone and ECF
1) parathyroid hormone
2) calcitriol
3) calcitonin
what does parathyroid hormone do?
- released with low Ca2+
- increase Ca & Pi in plasma by increasing kidney reabsorption, decreases Ca excretion, increases Pi excretion
- stimulates bone resorption
- stimulates calcitrol
what does calcitriol do?
- made in proximal tubule of kidney
- stimulates the reabsoption of Ca2+ and Pi by the kidney
- inhibits the excretion of Ca2+ and Pi
- stimulates bone resorption
what does calcitonin do?
- protects against high Ca2+
- stimulates bone formation (decreases plasma concentration of Ca2+) & the excretion of Ca2
- has same effect on Ca2+ and Pi
when do you see the spillover effect for phosphate?
when you have excess plasma Pi- plasma concentration at rest is super close to RPT, so any extra is filtered/excreted
glomerulotubular balance vs. tubuloglomerular feedback
GT balance- 67% of what’s put in is reabsorbed
vs
TG feedback- Na sensed by macula densa controls afferent arteriole and GFR
what is a non-volatile acid? what is a volatile acid?
- not derived from CO2 (H2CO3 is the ONLY volatile acid- can be excreted as gas by lungs)
what is a titratable acid and what is an example?
- any acid that will lose a proton at physologic pH (e.g. H2PO4-)- HPO4- combines with H+ in tubule
where is the majority of bicarb reabsorbed? how?
proximal tubule as H20 + CO2 when H+ is secreted
which buffer is able to adjust it’s quantity based on acidosis?
- ammonium- NH4
what happens in the distal tubule?
have no CA & most of bicarb has been reabsorbed so mostly have secretion of H+ via H+ K ATPase and H+ ATPase inserted with ISF is acidified
what is the difference between type 1 and type 2 RTA?
type 1- distal nephron doesn’t secrete H+, H+ goes back into blood
type 2- proximal tubule creates acidosis because low CA inhibits H+ recycling, HCO3- isn’t reabsorbed
how is bicarb regulated near RPT?
have HCO3-/Cl- antiporter in collecting duct
7 factors that regulate HCO3 reabsorption
1 GFR 2 Na balance 3 systemic acid-base balance 4 aldosterone 5 arterial K+ 6 arterial Cl- 7 ECV
3 forms of protons in urine
1 free hydrogen ions
2 titratable acids with HPO4-
3 diffusion trapped with NH4+
2 ways in which NH4 is secreted into collecting duct
1 non-ionic diffusion and trapping- NH3 follows H+ getting pumped into lumen
2 NH4- H+ antiporters in basolateral & apical membranes
how does hypokalemia influence pH?
- low K+ stimulates H+ secretion into tubule
- have H+/K+ antiporter on basolateral membrane, if K+ isn’t coming into cell, H+ won’t be put back into blood, will be extruded into tube instead
3 major systems that maintain plasma H+? which is fastest?)
1) chemical buffering
2) renal system (slow)
3) respiratory system (fast)
what is the henderson-hasselbach equation adjusted for renal?
pH= pKa + log (kidney- bicarb)/(lung- PCO2*0.03)
where is phosphate a weak buffer, and where is it stronger?
weak- blood
stronger- kidney
what is the assumed pKa of blood?
6.1
what is the difference between an open and closed buffer system?
- open- can easily get rid of acids (Co2 expiration, H+ excretion)
- closed- total concentration is fixed, just juggle between associated and dissociated forms (Hb, phosphate)
what happens to open system buffering power as pH decreases?
it increases exponentially, because pCO2 rises and that facilitates removal (closed system peaks where pH= pKa)
what is the isohydric principle?
when a solution contains more than 1 buffer, all buffer pairs are at equilibrium with the same proton concentration
normal pH
7.35-7.45
normal PaCO2
35-45
normal bicarb
22-28 mM
normal H+
35-45 nM
what is the compensation for metabolic acidosis?
- dec pH
- dec Co2
COMP: decrease CO2 more
what is the compensation for respiratory alkalosis?
- inc pH
- dec Co2
COMP: decrease HCO3
