acid base balance Flashcards
what is the pH range for life to operate
6.8-7.8 (apart from exceptional circumstances eg. stomach)
what is the optimal blood pH range
7.35-7.45
Ka equation
[H+][A-]/[HA]
what is pKa
a number that describes the acidity of a particular molecule -> calculated by -log(Ka)
what is a buffered solution
a solution in which the addition of an acid or base does not affect the pH of the solution
what are the main physiological buffers (4)
- bicarbonate (HCO3-) -> this is the main buffer
- phosphate (H2PO4 r=or HPO42-)
- plasma proteins
- haemoglobin
what is a volatile acid
an acid that can be excreted by the lungs i.e. CO2
what is the biocarbonate/CO2 chemical equaiton
CO2 + H2O <–(carbonic anhydrase)–> H2CO3 <–> H+ + HCO3-
the latter step occurs via rapid ionisation
what happens to the deconjugated form of H2CO3
H+ excreted by kidneys; HCO3- reabsorbed by kidneys
what are the 3 lines of defence against pH reduction
- bicarbonate
- replenishment of bicarb by kidneys
- removal of CO2
what is the net endogenous acid production
The nonvolatile acid load -determined by the balance of acid and alkali precursors in the diet
how many days could a person survive without the production of new bicarb
5 days
what is renal net acid excretion
the net amount of acid excreted in the urine per unit time - Its value depends on urine flow rate, urine acid concentration, and the concentration of bicarbonate in the urine
what is acidemia
an arterial pH below the normal range (<7.35)
what is alkalemia
an arterial pH above the normal range(>7.45)
what is acidosis
a process that tends to lower the extracellular fluid pH
what is alkalosis
a process that tends to raise the extracellular fluid pH
where is acid produced from in the body
tissue metabolism and diet
where is bicarbonate filtered/resorbed
filtered at the glomerulus, resorbed at the tubules
(and <0.1% excreted in the urine)
what is required to neutralise net endogenous acid production
reclamation of filtered bicarbonate and generation of new bicarb
where does the majority of the bicarb resorption occur
in the proximal convoluted tubules -> this also means that this is where the most H+ is secreted as for each HCO3- reabsorbed, 2H+ are released
bicarb resorption in the early tubular segments MOA (6)
- Na+/K+ ATPase results in build up of Na+ gradient extraceullularly in the renal peritubular fluid (3Na+ out, 2K+ in)
- this allows Na+ to move into the cell from the tubular lumen down its gradient (via Na+/H+ exchanger i.e. H+ out)
- HCO3- in the lumen bonds with H+ ion forming H2CO3
- this is then split into CO2 + H2O
- CO2 enters the cell where it is turned back into H2CO3 and then broken into HCO3-
- HCO3- excreted alongside Na+ via co transporter into the renal interstitial fluid (H+ then leaves cell via mech in step 2)
tubular lumen = filtrate from the glomerulus, interstitial fluid = blood
what transporter is responsible for moving HCO3- into the renal interstitial fluid in the distal tubular segments
Cl-/HCO3- exchangers (down their concentration gradients)
how is new bicarb generated in the kidneys
by product of ammoniagenesis
why does bicarb have to be split into CO2 + H2O in order to enter the tubular cells
HCO- is too polar of a molecule so cannot pass through the lipophilic cell membrane, while H2O and CO2 are not as polar
what is ammoniagenesis
the breakdown of amino acids (esp. glutamine) into ammonia -> triggered by acidosis
why are buffers essential in urine
they allow H+ ions to be excreted without the pH of urine dropping below 4.0
what is the normal urine pH range
4.5 - 8.0
how does ammonia buffer the urine MOA
- ammonia is lipid soluble so it diffuses freely into the tubule, where it combines with a hydrogen ion to form an ammonium NH4+ ion
- Ammonium NH4+ combines with chloride Cl- in the urine -> Because ammonium chloride is only weakly acidic, the urine pH doesn’t drop much even though it now contains a lot of hydrogen H+ ions
what is the secondary buffer system in the urine
phosphate
how does phosphate act as a buffer
- acidosis stimulates the excretion of urinary phosphate
- HPO4^2- + H+ -> H2PO4-, binding happens in the tubular lumen with H+ excreted via the Na+/H+ exchanger
- H2PO4 is then excreted in the urine
why is the byproduct of ammonia generation in ammoniagenesis
HCO3- -> this then enters the renal intersstitial lfuid
what would happen to blood/urinary bicarb conc if a carbonic anhydrase inhibiting drug was adminstered
bicarb cant be reabsorbed as carbonic anhydrase is required for HCO3- to enter the cell and for H2CO3 to be deconjugated =>
urinary bicarb - increased
blood bicarb - decreased
2 drugs which inhibit carbonic anhydrase
- acetazolamide (carbonic anhydrase inhibitor, used in glaucoma)
- topiramate (epilepsy, migraine)
what is the urine anion gap
[(Na+ + K+) – (Cl−)]
used to roughly estimate whether urine ammonium is increased or decreased in the evaluation of hyperchloremic metabolic acidosis
what is hyperchloremic metaboic acidosis
a pathological state that results from bicarbonate loss, rather than acid production or retention
what does a negative urine anion gap indicate
more chloride than cations -> another cation is being excreted e.g. NH4
what is the correct response to metabolic acidosis
increased renal ammonium excretion (-ve UAG)
what does a negative urine anion gap indicate about the cause for metabolic acidosis
the tubular function is intact => extra renal cause for metabolic acidosis
what does a positive urine anion gap indicate in metabolic acidosis
reduced renal ammonium excretion => reduced renal acid secretion -> renal tubular problem
3 causes of respiratory alkalosis
- congestive cardiac failure
- raised ICP
- hyperventilation
how is H+ secreted into the urine
- via Na+/H+ exchanger in the proximal convoluted tubule
- via H+ ATPase in the distal tubules
