Lecture 39: Renal Regulation of H+ Flashcards
what is normal ECF pH range
7.35-7.45
what is the typical pH of ICF
7.2
how do cells cope with lower pH
increased buffering
give 2 types of buffer systems
- chemical
- physiological
how do chemical buffers maintain pH
- present in all body fluids
- can bind to H+ removing it from solution if conc ^
- can release H+ if conc dec.
- first line defence agains pH changes
what is a physiological buffer
system that stabilises body fluid pH by controlling excretion of acids or bases (renal system) or volatile acids e.g. CO2 (resp system)
- can utilise chemical buffers as part of their pH control
compare the renal system and resp system as physiological buffers
Renal:
- greatest buffering capacity
- able to excrete large amounts of H+ ions
- takes several hours to a day to have significant effect on body fluid pH
Resp:
- less buffering capacity
- can only excrete volatile acids
- significant effect in just a few minutes
give examples of chemical buffers and compare
Protein
- present in ICF and ECF
- accounts for 75% of all chemical buffering in body
Bicarbonate
- present in ICF and ECF
- particularly important in pH regulation by kidneys
- CO2 + H2O H2CO3 H+ + HCO3-
outline how the kidney can increase or decrease body fluid pH
- excreting acidic/alkaline urine
- H+ and HCO3- filtered at glomerulus
- combine in filtrate –> H2CO3
- dissociates –> H20 + CO2 which both diffuse into tubular cell
- CO2 + H2O H2CO3 H+ + HCO3-
- HCO3- diffuses into blood, H+ secreted into filtrate
- secreted H+ recombines with HCO3- repeating cycle
describe the process of renal correction of acidosis
- acidosis (ECF <7.35 pH) –> excess H+
- all available HCO3- combine with H+
- any excess CO2 in filtrate (resp acidosis) also reabsorbed
- CO2 + H2O H2CO3 H+ + HCO3-
- HCO3- diffuses into blood to increase pH while H+ is secreted into filtrate
- no more HCO3- available so excess H+ excreted in urine (lower urinary pH)
- ECF pH returned to normal
describe what limits H+ secretion and how that affects HCO3- reabsorption
[H+] gradient
- pH below 4.5 (^ [H+] in filtrate) stops H+ secretion
- limits reabsorption of HCO3-
outline how H+ is buffered in urine
- ^ [H+] in filtrate
- NH3 secreted by tubular cells
- NH3 + H+ –> NH4+
- NH4+ isn’t reabsorbed (b/c charged) so H+ is excreted in urine
where does NH3 secreted by tubular cells come from
breakdown of protein and amino acids
what occurs in uncompensated acidosis
- dec. pH changes the binding of Ca2+ to plasma prots e.g. albumin
- more H+ binds to albumin –> more free Ca2+
- Ca2+ blocks Na+ channels and reduces their opening
- reduction in AP firing in myocytes and nerves
- resting MP of excitable cells stabilised making them harder to stimulate
- CV depression –> bradycardia leading to asystole
- CNS depression –> stupor followed by coma
give some causes of acidosis
- resp acidosis
- metabolic acidosis
- -> renal injury/disease
- -> aspirin overdose
- -> diabetic ketoacidosis
- -> alcoholism
- -> diarrhoea
- -> Addison’s disease
describe what is seen biochemically in the blood in resp acidosis
- ^ PaCO2 and dec. PaO2
- slightly low pH
- ^ plasma HCO3- (renal compensation
how does diarrhoea cause acidosis
- loss of Na+ in filtrate means less H+ secreted
- less HCO3- reabsorbed
how does Addison’s disease cause acidosis
- hypoaldosteronism
- dec. Na/H pump function
- dec. H+ secretion
- dec. HCO3- reabsorption
- lactic acid builds up
describe what is seen biochemically in the blood in metabolic acidosis
- low pH and low ECF [HCO3-]
- normal PaO2 and norm/dec. PaCO2
- Kussmaul’s breathing (compensatory deep breathing)
- as [H+] ^ and [HCO3-] dec. the gap between number of +ve and -ve ions (anion gap) ^
- -> indicative of underlying causes
describe the process of renal correction of alkalosis
- alkalosis (ECF pH >7.45)
- ^ [H+] (or dec [HCO3-]) in filtrate means less H2CO3 formed in tubular lumen
- less CO2 and H2O formed and reabsorbed
- thus less H2CO3 prod in tubular cells
- less HCO3- reabsorbed
- less H+ secreted while excess HCO3- excreted
- body continuously creates more H+ so plasma ^ [H+]
what occurs in uncompensated alkalosis
- ^ pH changes binding of Ca2+ to plasma prots
- less H+ binds to albumin so more Ca2+ binds to albumin (less ECF [Ca2+])
- relieves block of Na+ channels and ^ opening (^ membrane permeability to Na+)
- ^ AP firing in myocytes and nerves
- Em of excitable cells depolarises due to less free Ca2+
- confusion ensues, skeletal muscle spasms, death
give some causes of alkalosis and what would be seen biochemically
- respiratory alkalosis
- -> hyperventilation - dec. PaCO2 and HCO3- (renal comp)
- metabolic alkalosis
- -> bicarbonate (antacid) overdose - ^ HCO3- and ^ PaCO2 (resp comp)
- -> hyperaldosteronism - ^ H+ secretion
- -> vomiting - loss of gastric acids
compare renal and resp compensation in acidosis vs alkalosis
Acidosis:
resp comp
–> ^ CO2 blown off by lungs
renal comp
–> ^ HCO3- reab
Alkalosis:
resp comp
–> less CO2 blown off by lungs
renal comp
–> less HCO3- reab
