acid-base balance Flashcards by Marissa Bobay

pH range of ECF

7.35 - 7.45

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pH of ECF controlled by what 3 systems

-buffering

-resp system (removes CO2 from plasma)

-kidneys (excretes acidic/alkaline urine-> eventually changes pH of blood when parts are reabsorbed)

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what is the major buffer system used in the body

CO2 - carbonic acid - bicarbonate buffer system

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what is the CO2 - carbonic acid - bicarbonate buffer system; what is it catalyzed by

catalyzed by CA (carbonic anhydrase)- can catalyze 1st rxn in EITHER direction

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henderson-hasselback equation for bicarbonate buffers

pH = 6.1 + log ( [HCO3-] / alpha x Pco2)

pKa: 6.1
alpha: 0.03
Pco2: partial pressure of CO2

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in an ideal world, what is supposed to be the denominator for the henderson-hasselback equation for bicarbonate buffer, & what is used instead

carbonic acid (but can’t be measured bc it completely dissociates)

so we use->
alpha x Pco2

alpha: permeability coefficient for CO2

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what is the normal ratio of bicarbonate to alpha Pco2 at a pH of 7.4

[HCO3-] : alpha Pco2

20 : 1

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what is true about the concentrations of bicarbonate & CO2 if the ratio of bicarbonate : alpha Pco2 is 20:1

concentrations don’t matter, as long as ratio is 20:1, then pH = 7.4

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normal [HCO3-]

~24 mM

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normal (arterial) Pco2

40 mmHg

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normal amount of CO2/volatile acid produced per day

15,000 mmol /day

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normal amount of fixed acid produced per day

1 mmol / kg /day

(~70 kg man -> makes 70 mmol /day)

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what has to happen to all daily acid load, & why

all acid produced must be excreted -> to maintain acid-base homeostasis

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(for fixed acid)

intake + production = _____ + _____

excretion + elimination

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every day, kidneys must secrete enough H+ to _____ & _____

excrete ~70 mmol fixed acid
&
reabsorb the filtered ~4300 mmol HCO3-

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how much HCO3- is filtered & reabsorbed per day

4300 mmol /day

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H+ secreted into lumen of nephron is immediately buffered by one of 3 buffer systems:

1) reacts w filtered HCO3-
HCO3- + H+ -> CO2 + H2O

2) produces a titratable acid
B- + H+ -> HB

3) reacts w NH3 (ammonia)
NH3 + H+ -> NH4+

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3 bases commonly used in buffer system that produces a titratable acid

HPO42-
creatinine
urate

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when is HCO3- indirectly reabsorbed

when it reacts w secreted H+ in the tubular fluid (as one of the buffer systems)

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HCO3- (bicarbonate in TF that was filtered across glomerulus) reabsorption mechanism

NHE (apical membrane) secretes H+ into TF
->
H+ + HCO3- react & form H2CO3 (carbonic acid)
->
H2CO3 –(CA)–> CO2 + H2O
->
CO2 crosses apical membrane & goes into cell
->
CO2 + H2O –(CA)–> H2CO3
->
H2CO3 -> H+ + HCO3-
->
HCO3- crosses basolateral membrane & leaves cell

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3 steps for how body deals w non-volatile acid

1) ECF buffers immediately neutralize acid

2) if acid is buffered by HCO3-, resulting CO2 is excreted by lungs (this HCO3- needs to be replaced)

3) buffer regenerated by kidneys

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2 ways fixed acid (H+) is excreted

buffered by a “titratable acid”

buffered by NH4+ (ammonium)

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for every fixed acid (H+) that is buffered, what molecule is produced

HCO3-

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equation for net urinary acid excretion (UAE)

UAE = (H+ excreted as titratable acid) + [ammonia in urine] - (excretion of filtered HCO3-)

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why can you not just measure pH to get net urinary acid excretion (UAE)

pH is mostly [free H+] (and most of these are still buffered)

3 urinary buffers, & which is most important

HPO42- (phosphate- most important) urate creatinine

what is the pH from proximal tubule -> up through distal tubule, & what buffer works best here

tubular fluid pH is ~7 phosphate

how do you know what buffer will work best for a solution

if the pKa of the buffer is within 1 of the solution's pH

pH > pKa, _____ of the buffer is protonated

less

pH < pKa, _____ of the buffer is protonated

when are urate & creatinine good buffers

later in collecting duct as pH begins to fall

what is ammonia's behavior as a buffer & why

under normal conditions, majority of ammonia is protonated (becomes ammonium) bc it's pKa is 9.2

ammonia is produced by _____, & then secreted _____

epithelium in PCT cells secreted into tubular fluid

mechanism of ammonia production

(in PCT cells)

what is the key transporter in the apical membrane of the PCT for H+ secretion, & what is the secondary transporter

NHE3 (Na+/H+ exchanger) H+ ATPase

what is the key transporter in the basolateral membrane of the PCT for H+ secretion, & what are the other 2

NBCe1 (Na+/HCO3- cotransporter) AE2 (HCO3-/Cl-) Na+/K+ ATPase

locations on the nephron where there is NO acid-base handling

thin descending limb (tDLH) thin ascending limb (tALH)

what % of filtered HCO3- is reabsorbed in TALH

10%

what % of filtered HCO3- is reabsorbed in PCT

80%

what % of fixed acid is excreted in PCT

78% (as NH3 with some TA (titrated acid))

what % of filtered HCO3- is reabsorbed in distal tubule, CCD, & OMCD

10%

what % of fixed acid is reabsorbed in distal tubule, CCD, & OMCD

7% (as TA)

what % of fixed acid is reabsorbed in IMCD

15% (as TA)

what 2 molecules are reabsorbed at TALH

HCO3- NH4+

at TALH -intracellular production of _____ -apical secretion of _____ -basolateral efflux of _____

-production of H+ & HCO3- (from CO2 using CA) -apical secretion of H+ via NHE3 -basolateral efflux of HCO3- via AE2

in TALH, what can NH4+ be mistaken as & what happens bc of this

NH4+ can be mistaken as K+ -> & enter cell via ROMK or NKCC by posing as K+ -> then becomes NH3 in cell -> diffuses across basolateral membrane as NH3 into ECF

possible fates of NH3 after diffusing across basolateral membrane into ECF from TALH

1) diffuse into tDLH (passive secretion) 2) picked up by vasa recta & "washed out" into systemic circulation 3) secreted into MCD (medullary collecting duct) & titrated by H+ -> becomes NH4+ again & is excreted (most common route)

where does the greatest degree of acidification of TF occur in the nephron, & why is this surprising

in the collecting duct surprising bc most H+ secretion occurs in PCT (but pH doesn't change much bc H+ immediately taken care of)

why does most acidification occur in collecting duct

bc not much buffer is left to deal w H+

decreases in ratio [HCO3-] : alpha Pco2, _____ pH

decreases

increases in ratio [HCO3-] : alpha Pco2, _____ pH

increases

a change in arterial pH due to change in Pco2, is what kind of acid-base disturbance

respiratory

respiratory acid-base disturbances are usually caused by _____

changes in rate of CO2 exhalation (pulmonary CO2 excretion rate)

hypoventilation leads to _____

respiratory acidosis (retaining CO2)

hyperventilation leads to _____

respiratory alkalosis (expelling CO2)

normal range for arterial Pco2

35 - 45 mmHg

2 ways that kidneys respond to respiratory acidosis

-increase [HCO3- in ECF] (by increasing amount of filtered HCO3- that is reabsorbed) -increase new HCO3- production (by increasing rate of H+ secretion)

mechanism of kidney response to ACUTE respiratory acidosis

CO2 diffuses into cells from ECF -> lowers intracellular pH -> increases H+ (& HCO3-) secretion

mechanism of kidney response to CHRONIC respiratory acidosis

same effects as acute &... upregulates gene expression of transporters -> increases maximum rate of transport & HCO3- reabsorption

a change in arterial pH due to change in [HCO3-], is what kind of acid-base disturbance

metabolic

normal range of arterial [HCO3-]

22 - 28 mEq/L

diarrhea can cause _____ bc _____

metabolic acidosis loss of HCO3- in diarrhea

vomiting can cause _____ bc _____

metabolic alkalosis loss of H+ in vomit

mechanism of kidney response to ACUTE metabolic acidosis

(same as response to acute respiratory acidosis) CO2 diffuses into cells from ECF -> lowers intracellular pH -> increases H+ (& HCO3-) secretion

general kidney response to CHRONIC metabolic acidosis

makes new HCO3- (primarily through ammonia production)

mechanism of kidney response to CHRONIC metabolic acidosis

decreased ECF pH -> decreased ICF pH -> induces 2+ intra-cellular pathways 1) protein kinase C 2) tyrosine kinase -> signals go to nucleus -> increased expression of NHE3, NBC, ammoniagenic enzymes

what is the primary way the body gets rid of excess acid & makes new bicarbonate

production of ammonia

more urinary NH3/NH4+ = _____ new HCO3- produced

what is "volume contraction"

a decrease in effective circulating volume (ECV)

what do the compensatory responses to a decreased ECV lead to

secondary metabolic alkalemia

mechanism of secondary metabolic alkalemia

decreased ECV (volume contraction) -> RAAS system stimulated (goal = to bring more salt/water into body) -> increases angiotensin II & aldosterone -> angiotensin II increases H+ secretion via NHE (which increases HCO3- reabsorption & new HCO3- production) -> aldosterone stimulates: 1) H-ATPase in alpha-intercalated cells = H+ secretion (& HCO3- production) 2) K+ secretion = hypokalemia

(interrelationship between [H+ in ECF] & hyper-/hypokalemia) acidosis in ECF may induce a _____ in ECF

secondary hyperkalemia H+ in ECF < H+ in cell -> K+ in ECF > K+ in cell

(interrelationship between [H+ in ECF] & hyper-/hypokalemia) alkalosis in ECF may induce a _____ in ECF

secondary hypokalemia H+ in ECF > H+ in cell -> K+ in ECF < K+ in cell

why does the interrelationship between [H+ in ECF] & hyper-/hypokalemia exist

bc the cell is unintentionally trying to remain balanced with its + charges

(interrelationship between [H+ in ECF] & hyper-/hypokalemia) hypokalemia in cell may induce a _____ in cell, bc of _____

secondary alkalosis bc of H+ influx into cell K+ in cell < K+ in ECF -> H+ in cell > H+ in ECF

(interrelationship between [H+ in ECF] & hyper-/hypokalemia) hyperkalemia in cell may induce a _____ in cell, bc of _____

secondary acidosis bc of H+ efflux out of cell K+ in cell > K+ in ECF -> H+ in cell < H+ in ECF

interrelationship between [H+ in ECF] & hyper-/hypokalemia occurs in what cells

all cells of the body (systemic AND renal)