16. Renal Control of Acid-Base Balance Flashcards

1
Q

what change in pH will double or half [H]

A

change 0.3 pH

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2
Q

what are the body buffer systems

A

bicarb

Hb

Phosphate

plasma protein

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3
Q

what is pKa

A

pH at wich buffer is half saturated

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4
Q

How is H+ buffered by Hb & plasma proteins

A

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

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5
Q

How does buffering of H+ occur in acidemia when exchanging K+

A

if acidemia - low ECF pH

–>K/H exchange -> increase K+ ECF & increase H+ in ICF

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6
Q

how does buffering with H-K exchange happen during alkalemia

A

if alkalemia - high ECF pH

–>K/H exchange -> increase H+ ECF & increase K+ in ICF

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7
Q

henderson-hasselbalch equation to detect pH in body

A

[HCO3-] controlled by kidneys - slowly (large capacity)

PCO2 controlled by lungs - fast (limited capacity)

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8
Q

how does ventilation rate affect pH

A

breathe faster - less CO2 –> less H+ –> higher pH

hold breath - more CO2 –> more H+ –> lower pH

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9
Q

what is the clearance of glucose & HCO3-

A

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

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10
Q

what happens at the tip of the countercurrent exchange capillary loop

A

as flow downward -h2o reabs –> become more concentrate

flow becomes sluggish at tip to keep salty

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11
Q

what is the countercurrent multiplier

A

operates in the TAL

provide solute hypertonic renal medullary interstium while simulataneously diluting tubular fluid

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12
Q

what type of reabs happens at PT

A

2/3 of filtered solutes selectively reabsed

2/3 of filtered h2o reabsed

==> iso-osmotic tubular fluid reabs

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13
Q

what occurs at the thin descending limb and thin ascending loop

A

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

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14
Q

what happens at the TAL

A

urea is trapped

Na, Cl out and flow down into medullary interstitum

no h2o movement

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15
Q

what is the tubular fluid like after TAL

A

hypotonic tubular fluid

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16
Q

how does tubular fluid become dilute again in DCT

A

selective reabs of Na, Cl by Na-Cl cotransporter

17
Q

what/where does the final finetuning of Na reabs happen

A

aldosterone regulated Na/K exchange in CCT

18
Q

what does dilute urine contain

A

16% filtered h2o load

1% filtered NaCl load

& rest of solute = waste

19
Q

how/where does urine become concentrated

A

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

20
Q

How is bicarb reabsed in the PT

A
  1. Na/H antiporter on luminal side - Na in & H out
  2. H out & react with bicarb –> h2co3
  3. use carbonic anhydrase to make CO2
  4. CO2 freely cross apical mem
  5. combine w/ h2o in cell & use CA to make HCO3 & H
  6. HCO3 out of basolat side via Na/HCO3- symporter & recycle H+ w/ Na/H antiporter
21
Q

what increases H+ secretion

A

primary - decrease plasma HCO3-, increase PaCO2

secondary - increase filtered load of HCO2-, angiotensin II &/or aldosterone, decrease ECF vol &/or plasma [K}

22
Q

what decreases H+ secretion

A

primary - increase plasma HCO3, decrease PaCO2

secondary - decrease filtered load of HCO3- &/or aldosterone, increase ECF & plasma [K]

23
Q

how is H+ buffered by phosphate

A

secrete H+ distal nephron

bind NaHPO4- –> NaH2PO4

help regenerate plasma HCO3- that was consumed else where

*PO43- limited - so need ammonia for additional buffering*

24
Q

how is ammonia produced & used as a buffer

A

PT takes glutamine –> cleave into NH4+

metabolize –> NH3 - diffuse into PCT

–> convert back to NH4+

travel thru nephron –> NH3 into CCT

combine w/ H

25
Q

Where is HCO3- reabs in the CCT

A

alpha-intercalating cell

H+ out cell via K/H ATPase

–> combine w/ HCO3 - in lumen –> convert to CO2 using CA

CO2 back into cell –> convert to HCO3- & H+

HCO3- reabs via HCO3-/Cl- antiporter

26
Q

how is HCO3- secreted in the CCT

A

if too much HCO3-

secrete out at beta-intercalated cell

27
Q

how do you calculated Net Acid Excretion

A

= nonvolatile acid production each day to maintain acid-base balance

TA = salts of primarily phosphate, creatinine

28
Q

what is Renal Tubular Acidosis (RTK) type 1

A

impaired distal H secretion

<10-15 plasma HCO3-

urine pH > 5.5

low plasma K - correct w/ alkali therapy

b/c autoimmune disorder, hypercalciuria, sickle cell anemia, cirrhosis

29
Q

what is RTA type 2

A

impaired proximal HCO3- reabs

12-20 plasma HCO3-

<5.5 urine pH

low K - worsened by alkali therapy

-fanconi, multiple myeloma, drugs

30
Q

what is RTA type 4

A

lack of aldo or failure of kidney to respond

> 17 HCO3-

urine pH <5.5

high K+

= diabetic nephropathy, spironolactone, NSAIDS, chronic interstitial nephritis