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GERR > Lecture 39: Renal Regulation of H+ > Flashcards

Lecture 39: Renal Regulation of H+ Flashcards

1
Q

what is normal ECF pH range

A

7.35-7.45

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2
Q

what is the typical pH of ICF

A

7.2

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3
Q

how do cells cope with lower pH

A

increased buffering

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4
Q

give 2 types of buffer systems

A
  • chemical

- physiological

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5
Q

how do chemical buffers maintain pH

A
  • 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
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6
Q

what is a physiological buffer

A

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
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7
Q

compare the renal system and resp system as physiological buffers

A

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
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8
Q

give examples of chemical buffers and compare

A

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-
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9
Q

outline how the kidney can increase or decrease body fluid pH

A
  • excreting acidic/alkaline urine
  1. H+ and HCO3- filtered at glomerulus
  2. combine in filtrate –> H2CO3
  3. dissociates –> H20 + CO2 which both diffuse into tubular cell
  4. CO2 + H2O H2CO3 H+ + HCO3-
  5. HCO3- diffuses into blood, H+ secreted into filtrate
  6. secreted H+ recombines with HCO3- repeating cycle
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10
Q

describe the process of renal correction of acidosis

A
  • 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
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11
Q

describe what limits H+ secretion and how that affects HCO3- reabsorption

A

[H+] gradient

  • pH below 4.5 (^ [H+] in filtrate) stops H+ secretion
  • limits reabsorption of HCO3-
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12
Q

outline how H+ is buffered in urine

A
  • ^ [H+] in filtrate
  • NH3 secreted by tubular cells
  • NH3 + H+ –> NH4+
  • NH4+ isn’t reabsorbed (b/c charged) so H+ is excreted in urine
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13
Q

where does NH3 secreted by tubular cells come from

A

breakdown of protein and amino acids

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14
Q

what occurs in uncompensated acidosis

A
  • 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
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15
Q

give some causes of acidosis

A
  • resp acidosis
  • metabolic acidosis
  • -> renal injury/disease
  • -> aspirin overdose
  • -> diabetic ketoacidosis
  • -> alcoholism
  • -> diarrhoea
  • -> Addison’s disease
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16
Q

describe what is seen biochemically in the blood in resp acidosis

A
  • ^ PaCO2 and dec. PaO2
  • slightly low pH
  • ^ plasma HCO3- (renal compensation
17
Q

how does diarrhoea cause acidosis

A
  • loss of Na+ in filtrate means less H+ secreted

- less HCO3- reabsorbed

18
Q

how does Addison’s disease cause acidosis

A
  • hypoaldosteronism
  • dec. Na/H pump function
  • dec. H+ secretion
  • dec. HCO3- reabsorption
  • lactic acid builds up
19
Q

describe what is seen biochemically in the blood in metabolic acidosis

A
  • 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
20
Q

describe the process of renal correction of alkalosis

A
  • 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+]
21
Q

what occurs in uncompensated alkalosis

A
  • ^ 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
22
Q

give some causes of alkalosis and what would be seen biochemically

A
  • 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
23
Q

compare renal and resp compensation in acidosis vs alkalosis

A

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

GERR (46 decks)

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