Acid Base balance Flashcards
Describe the consequences of having plasma pH > 7.45. (5)
Alkalaemia
Very dangerous because reduces the soluability of calcium salts causing free Ca2+ to leave the ECF creating hypocalcaemia, which makes nerves more excitable, causing paraesthesia and tetany.
Describe the consequences of having plasma pH < 7.35. (5)
Slightly less dangerous.
Affects enzyme function, leading to potassium leaving cells.
Hyperkalaemia can be fatal because it affects muscle excitability, causing arrthymias.
Explain why retaining HCO3- in the kidney is important. (4)
Because correcting acidosis / alkalosis depends on changing the secretion of HCO3-
Because HCO3- is freely filtered, in alkalosis, more can be excreted and in acidosis, more can be retained or created by the kidneys, which then needs the spare H+ secreting.
Describe two methods of moving HCO3- from the epithelial cell into the blood in the PCT. (8)
Na+/H+ exchanger pumps H+ out where it binds to filtrate HCO3- forming H2O and CO2 which diffuse into cells forming H+ and HCO3- again. H+ is pumped out into filtrate, HCO3- diffuses into interstitium.
Glutamine in the cell > NH3 + H+ + alpha-ketoglutarate > NH4+ + 2HCO3-
NH4+ is a safer way to excrete H+ in the urine, HCO3- diffuses into the interstitium.
Describe moving HCO3- into the interstitium in DCT. (5)
Intercollated cells.
H2O and CO2 diffuse into the cell and form HCO3- and H+.
H+ is actively pumped out as Na+ gradient here is too small to power it like that.
H+ Binds to buffer of (HPO4)2- and is removed.
HCO3- moves into the interstitium via a Cl- / HCO3- exchanger.
Describe the relationship between potassium and HCO3- reabsorption. (3)
In hyperkalaemia, the kidney can’t reabsorb or create HCO3- as well.
Hypokalaemia - metabolic alkalosis
Hyperkalaemia - metabolic acidosis
Describe compensation. (4)
When the body changes something to get the HCO3- : p(CO2) ratio normal again. Complete compensation is when pH is back in normal range.
Uncompensated is when only the thing causing the problems is abnormal
Partial compensation is when both things are errant but pH is still outside normal range.
Describe the anion gap. (3)
The difference between the concentrations of MEAURED anions and cations.
( [Na+] + [K+] ) - ( [Cl-] + [HCO3-] )
Normally 10-18 mmol/l due to unmeasured anions like lactate.
Describe metabolic acidosis with altered anion gap. (3)
If a metabolic acid like lactic acid releases H+ It reacts with HCO3- in the blood, removing HCO3- and replacing it with lactate, an anion not measured.
Describe metabolic acidosis with preserved anion gap. (4)
Renal causes of acidosis
Anion gap unchanged because HCO3- / Cl- antiporter doesn’t work, so no HCO3- moves into plasma, but no Cl- leaves either.
Cl- is measured in the anion gap, so it is unchanged.
Describe respiratory acidosis. (4)
Caused by type 2 respiratory failure (COPD, asthma, drug reaction) Increased p(CO2) (and decreased p(O2)) due to improperly ventilated alveoli. Body raises [HCO3-] to compensate.
Describe respiratory alkalosis (4)
Caused by hyperventilation (anxiety or chronic hypoxia in type 1 Resp failure) Decreased p(CO2) due to trying to maintain p(O2). Body lowers [HCO3-] to compensate.
Describe metabolic acidosis with Increased anion gap. (4)
Caused by metabolic production of acid like lactic acidosis, diabetic ketoacidosis.
Decreased [HCO3-] because it’s reacted with H+ and been replaced with another anion.
Body lowers p(CO2) to compensate.
Describe metabolic acidosis with maintained anion gap. (4)
Caused by renal failure where the kidney can’t excrete H+, or when chronic diarrhoea washes away all the HCO3- so the HCO3- / Cl- antiporter stops.
Decreased [HCO3-].
Body lowers p(CO2) to compensate.
Describe metabolic alkalosis. (4)
HCO3- is retained over Cl-.
Caused by severe loss of H+ (vomiting), or hypokalaemia.
Want to excrete [HCO3-] to fight, but often volume depleted, so Na+ retention excreted the H+ needed to excrete HCO3-.
Cannot compensate - cannot breathe less to raise p(CO2) because p(O2) would fall.