16. Renal Control of Acid-Base Balance Flashcards
what change in pH will double or half [H]
change 0.3 pH
what are the body buffer systems
bicarb
Hb
Phosphate
plasma protein
what is pKa
pH at wich buffer is half saturated
How is H+ buffered by Hb & plasma proteins
CO2 dissolved, bound to Hb
-bind H20 –> make H2CO3 and dissociate into HCO3- and H+ –> HCO3- out of RBC & H+ binds Hb
HbO2 dissociate when O2 out to tissues & Hb binds CO2 & H+
plasma -CO2+protein + NH2 –> protein-NHCOO+H
How does buffering of H+ occur in acidemia when exchanging K+
if acidemia - low ECF pH
–>K/H exchange -> increase K+ ECF & increase H+ in ICF
how does buffering with H-K exchange happen during alkalemia
if alkalemia - high ECF pH
–>K/H exchange -> increase H+ ECF & increase K+ in ICF
henderson-hasselbalch equation to detect pH in body
[HCO3-] controlled by kidneys - slowly (large capacity)
PCO2 controlled by lungs - fast (limited capacity)
how does ventilation rate affect pH
breathe faster - less CO2 –> less H+ –> higher pH
hold breath - more CO2 –> more H+ –> lower pH
what is the clearance of glucose & HCO3-
glucose - should be 0 bc reabs all
HCO3- almost 0 bc reabs almost all
clearange = flow rate - how much plasma needed to take solute out
what happens at the tip of the countercurrent exchange capillary loop
as flow downward -h2o reabs –> become more concentrate
flow becomes sluggish at tip to keep salty
what is the countercurrent multiplier
operates in the TAL
provide solute hypertonic renal medullary interstium while simulataneously diluting tubular fluid
what type of reabs happens at PT
2/3 of filtered solutes selectively reabsed
2/3 of filtered h2o reabsed
==> iso-osmotic tubular fluid reabs
what occurs at the thin descending limb and thin ascending loop
thin descending - h2o reabs & diffuse Na, Cl in bc gradient
==> passage of tubular fluid down into hypertonic renal medulla
generation of hypertonic tubular fluid
thin ascending- no h2o movement & Na,Cl diffuse out bc gradient
what happens at the TAL
urea is trapped
Na, Cl out and flow down into medullary interstitum
no h2o movement
what is the tubular fluid like after TAL
hypotonic tubular fluid
how does tubular fluid become dilute again in DCT
selective reabs of Na, Cl by Na-Cl cotransporter
what/where does the final finetuning of Na reabs happen
aldosterone regulated Na/K exchange in CCT
what does dilute urine contain
16% filtered h2o load
1% filtered NaCl load
& rest of solute = waste
how/where does urine become concentrated
ADH make late DT and CCT more permeable to h2o
increase reabs
end up w/ <0.2% h2o filtered load, less than 1% NaCl filtered load & rest = waste
How is bicarb reabsed in the PT
- Na/H antiporter on luminal side - Na in & H out
- H out & react with bicarb –> h2co3
- use carbonic anhydrase to make CO2
- CO2 freely cross apical mem
- combine w/ h2o in cell & use CA to make HCO3 & H
- HCO3 out of basolat side via Na/HCO3- symporter & recycle H+ w/ Na/H antiporter
what increases H+ secretion
primary - decrease plasma HCO3-, increase PaCO2
secondary - increase filtered load of HCO2-, angiotensin II &/or aldosterone, decrease ECF vol &/or plasma [K}
what decreases H+ secretion
primary - increase plasma HCO3, decrease PaCO2
secondary - decrease filtered load of HCO3- &/or aldosterone, increase ECF & plasma [K]
how is H+ buffered by phosphate
secrete H+ distal nephron
bind NaHPO4- –> NaH2PO4
help regenerate plasma HCO3- that was consumed else where
*PO43- limited - so need ammonia for additional buffering*
how is ammonia produced & used as a buffer
PT takes glutamine –> cleave into NH4+
metabolize –> NH3 - diffuse into PCT
–> convert back to NH4+
travel thru nephron –> NH3 into CCT
combine w/ H
