Chemical control of pH & acid base balance Flashcards

1
Q

What is the bodies response to metabolic acidosis?

A

hyperventilation to blow of more co2 so decrease pCO2 and so decrease pH

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2
Q

What pneumonic can be used to be able to interpret acid- base status?

A
ROME - respiratory opposite (if pH high and CO2 low or pH low and CO2 high then its a respiratory cause)
Metabolic equal (if pH low and HCO3- low or pH high and HCO3- high then metabolic cause?
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3
Q
What is the interpretation for these ABG and blood results:
- pH low 
- CO2 high 
- HCO3- normal
Give a likely cause
A

Uncompensated respiratory acidosis

Hypoventilation due to drug OD, type 2 resp failure

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4
Q

Why are respiratory acidosis and metabolic alkalosis hard to compensate for?

A

Respiratory acidosis compensation requires the kidneys to increase HCO3 recovery and produce more HCO3, this takes time.
Metabolic alkalosis compensation requires hypoventilation, which can only be done to an extent and doesn’t decrease CO2 very significantly

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5
Q

Interpret these results:

  • pH low end of normal
  • pCO2 low
  • HCO3- low
A

compensated metabolic acidosis
- Metabolic acidosis eg due to anaerobic respiration has decreased HCO3-, but body has compensated by increasing ventilation rate to decrease pCO2 and bring the pH to normal again

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6
Q

What to the peripheral chemoreceptors detect? where are they found? what do they do when stimulated?

A
  • they detect large falls in O2
  • theyre found in the carotid body and aortic arch
  • they increase breathing rate, increase heart rate, change blood flow distribution (more to brain, heart and kidneys)
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7
Q

Where are central chemoreceptors found?

A

the CSF of the medulla of the brain

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8
Q

What do central chemoreceptors detect and how?

A

They detect pH but only pH changes due to plasma pCO2 changes. This is because H+ and HCO3- cannot enter the CSF but pCO2 can. Therefor increases in blood pCO2= decreases in blood and CSF ph= detection by central chemoreceptors= hyperventilation to blow excess co2 off.

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9
Q

How will persistant increases in pCO2 (COPD) affect the central chemoreceptors?

A

The choroid plexus cells will increase HCO3- production to ensure the CSF pH remains within normal range. The chemoreceptors will therefor reset as pH is normal- pCO2 is still high but accepted as normal and ventilation rate will remain the same.

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10
Q

How much more CO2 is in blood than O2?

A

2.5x more

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11
Q

What happens when you add more CO2 to blood?

A

It reacts with H20 forming carbonic acid, which quickly dissociates to form H+ making the blood more acidic (pushes equilibrium to the right)

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12
Q

How can henderson hasselbalch equation be used to calculate blood pH?

A

pH= pK + log( [hco3-]/ (pCO2 x 0.23))
0.23 is solubility coefficient of CO2, so gives us [CO2]
pK is 6.1 for this reaction at 37 degrees

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13
Q

How much greater is the concentration of HCO3- in the blood than CO2 in the blood?

A

20x

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14
Q

How can RBCs create HCO3- when pCO2 increases?

A

CO2 increases in blood and so also RBCs, this drives production of HCO3 and H+ by reaction with water (catalysed by carbonic anhydrase). The RBC binds the H+ produced to negatively charged H+.
The HCO3- produced is expelled from the RBC via the chloride/ bicarbonate exchanger. Therefor increase in pCO2= increase in HCO3- production from RBCs.

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15
Q

In what state is Hb able to bind with H+?

A

In T state- low O2- at tissues. This is also where pCO2 is highest, and so RBCs are able to produce more HCO3- in response to this.
At lungs, it goes back to R state as O2 binds, the H+ is released, which reforms CO2 again which is blown off.

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16
Q

Other than H+ transport on CO2 and in dissolved state, how else is CO2 transported to the lungs?

A

Bound to proteins such as Hb (carbaminocompounds).

17
Q

By how much does CO2 increase from arterial to venous blood?

A

8%- therefor 92% of CO2 in blood is being used to for pH buffering and only 8% has been produced by respiration and is being transported

18
Q

What may cause respiratory alkalosis?

A

hyperventilation- panic attacks, long term hypoxia (type 1 resp failure)

19
Q

What may cause metabolic acidosis?

A
  • Renal failure (high urea)
  • Renal tubular acidosis (rare, H+ not excreted and HCO3- not reabsorbed)
  • Anaerobic respiration
  • Severe persistant diarrhoea (HCO3- lost)
20
Q

What is the anion gap and what is it useful for?

A

The amount of Na+ and K+ minus the amount of Cl- and HCO3-.
The gap increases if HCO3- is replaced by anions other than Cl- (lactic acid).
If there is a renal cause of the metabolic acidosis then the anion gap will be normal, as HCo3- is replaced by Cl-.
If diarrhoea caused the metabolic acidosis the anion gap is also normal because HCO3- is replaced by Cl- here too.

21
Q

What can cause metabolic alkalosis?

A
  • vomiting
  • K+ depletion
  • loop and thiazide diuretics
22
Q

How is HCO3- recovered in the PCT?

A

NHE extrudes H+ into lumen, this reacts with HCO3- to make CO2 and H20, which enter epithelial cell by diffusion, where HCO3- and H+ reform, the NHE extrudes the H+ again and HCO3- put into blood by cotransport with Na+.

23
Q

How is HCO3- created in the proximal tubule when acidosis detected?

A

glutamine is converted to a- ketogluterate, this produces 2x HCO3- and 2x NH4. The NH3+ moves into lumen where it reacts with H+ to make NH4 (buffers it) and theyre excreted (increases excretion of H+).

24
Q

How is more H+ excreted/ more HCO3- made in the distal tubule when acidosis detected?

A

H20 and CO2 (from respiration) react to create H+ which is extruded into lumen by ATPase and buffered by NH3 and HPO4. The HCO3- is extruded into blood.

25
Q

How does hyperkalaemia lead to metabolic acidosis?

A
  • Increased K+ entry into cells= increased H+ leaving cells
  • also K+/H+ exchanged on apical side of tubular cells in kidney increases to excrete more K+, this means more H+ recovery in kidneys and more HCO3- excretion
26
Q

How does acidosis lead to hyperkalaemia?

A

More H+ enters cells so more K+ leaves and causes hyperkalaemia

27
Q

How does hypokalaemia lead to alkalosis?

A

K+ moves out and H+ moves into the cell, less H+ in interstitium= alkalosis

28
Q

What does alkalosis do to calcium?

A

It causes increased Ca2+ binding to proteins, which decreases ironised (free/ active) calcium, which causes hypocalcamia, making neurones more excitable, paaresthesia and tetany.
Acidosis does the opposite

29
Q

How does the kidney reduce plasma HCO3- in metabolic alkalosis?

A

plasma HCO3- increase means more is filtered, the Tm for HCO3- is exceeded and more is excreted