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Urinary - Physiology > Acid Base Balance > Flashcards

Acid Base Balance Flashcards

1
Q

why is blood pH important

A

enzymes and metabolic reactions are sensitive to pH

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2
Q

normal pH and H+ concentration of blood

A

7.4 and 40x10-6 mmoles/L

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3
Q

how does respiration produce acid

A

CO2 + H2O = H2CO3 = HCO3- and H+

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4
Q

acids of the metabolism

A

fatty acids, lactic acid, phosphoric acid, amino acids with sulphur

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5
Q

what is the purpose of a buffer

A

to minimize pH changes when H+ ions are added or removed

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6
Q

what is the main buffer system in ECF

A

bicarbonate buffer system

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7
Q

what are the extracellular buffers

A

bicarbonate, plasma protein and dibasic phosphate

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8
Q

what tissue holds an additional store of buffer

A

bone –> carbonate

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9
Q

when would the bone’s carbonate store be useful

A

when there is an acid load in renal failure and the kidneys can’t compensate

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10
Q

why does acidosis lead to hyperkalaemia

A

increased H+ being moved into cell to be buffered requires K+ to move out to maintain electrochemical neutraility

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11
Q

buffering of metabolic acids

A

43% in plasma, 57% in cells by HCO3-

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12
Q

buffering of respiratory acids

A

97% in cells by HCO3- and Hb, 3% in plasma

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13
Q

pH is proportional to

A

concentration of HCO3- /partial pressure of CO2

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14
Q

how do the kidneys regulate pH

A

by reabsorbing and creating HCO3-

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15
Q

process of HCO3- reabsorption

A
  1. H+ actively secretion into tubule lumen
  2. Na+ reabsorbed to maintain electrochemical
  3. filtered HCO3- + H+ = H2CO3
  4. carbonic anhydrase breakes into water and CO2
  5. these freely move into cell
  6. carbonic anhydrase form them back into H2CO3
  7. dissociate into H+ and HCO3-
  8. HCO3- moved into blood either by co transport with Na+ or by swapping with Cl-
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16
Q

why can’t we excrete free H+ ions

A

because that would mean a pH of 1. That would sting to pee out

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17
Q

main buffers of urine

A

dibasic phosphate, uric acid and creatinine

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18
Q

difference between H+ pumping into tubule lumen in proximal tubule and distal and collecting

A

in proximal tubule –> sodium hydrogen countertransporter

in distal and collecting duct –> ATP pump for H+

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19
Q

excretion of H+ by HPO42-

A

NaHPO4 in lumen loses its Na+ in exchange for H+

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20
Q

where does most H+ excretion occur and why there

A

mostly in distal tubule because that’s where phosphate ions not reabsorbed by proximal Tm mechanism become most concentrated by the removal of volume of filtrate

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21
Q

excretion of H+ by ammonium

A

NH3 made from glutamine –> moves out into tubule lumen –> combines with H+ –> NH4+ combines with Cl- –> NH4Cl- is excreted

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22
Q

NH3 is lipid/water soluble

A

lipid

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23
Q

what amino acid is NH3 made from

A

primarily glutamine

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24
Q

what enzyme makes glutamine into glutamate to produce NH3

A

renal glutaminase

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25
Q

true/false NH4+ formed in cell can be pumped out into lumen by exchanging with Na+

A

true

26
Q

where is ammonium ion mostly formed (i.e. combined with H+) in the proximal tubule

A

in the cell, it is then pumped into lumen by exchanging with Na+

27
Q

where is ammonium ion mostly formed (i.e. combined with H+) in the distal tubule

A

in the lumen

28
Q

effect of high intracellular pH on renal glutaminase

A

reduced renal glutaminase activity

29
Q

effect of low intracellular pH on renal glutaminase

A

increased renal glutaminase activity, to excrete the increased H+

30
Q

what is the main adaptive response of the kidneys in response to acidosis

A

to increase NH4+ production through renal glutaminase and excrete more H+

31
Q

how long does it take for the kidneys to have their maximal effect in response to acidosis

A

4-5 days

32
Q

why does it take the kidneys so long to compensate for acidosis/alkalosis

A

because of the requirements of the increase in protein synthesis/switch off the ability to make NH4+

33
Q

how much H+ can be excreted at maximum in acidosis per day

A

250mmoles/L

34
Q

causes of respiratory acidosis

A

drugs - barbituates, opiates

other - obstruction, empysema, asthma, bronchitis

35
Q

effect of PCO2 on HCO3- reabsorption

A

increases ability to reabsorb

36
Q

effect of hyperventilation on pCO2

A

reduces it –> increased ventilation blowing off more CO2

37
Q

causes of respiratory alkalosis

A

hyperventilation, aspirin, high altitude

38
Q

how does high altitude affect blood pH

A

at high altitudes the low O2 stimulates peripheral chemoreceptors to increase ventilation. More CO2 is blown off meaning less H+ –> alkalosis

39
Q

origin of a metabolic acidosis

A

reduced HCO3- conc

40
Q

causes of metabolic acidosis

A

increased H+ production (ketoacidosis), failure to excrete H+, loss of HCO3- in diarrhoea

41
Q

process of metabolic acidosis

A

reduced HCO3- –> increased H+ –> stimulation of ventilation –> blow off CO2 –> less H+ made

42
Q

renal response to metabolic acidosis

A

takes some time to increase H+ excretion and generate new HCO3-

43
Q

true/false in metabolic acidosis/alkalosis respiratory compensation delays renal correctionbut protects the pH

A

true

44
Q

origin of metabolic alkalosis

A

increase in HCO3-

45
Q

causes of metabolic alkalosis

A

vomiting (h+ loss), excess H+ excretion (aldosterone and liquorice), blood transfusions

46
Q

how do blood transfusions cause metabolic alkalosis

A

the anticoagulant citrate converts to bicarbonate

47
Q

acid base disorder of ketoacidosis

A

metabolic acidosis

48
Q

acid base disorder of bronchitis

A

chronic respiratory acidosis

49
Q

what is the risk from hyperkalaemia

A

ventricular fibrillation

50
Q

acid base disorder of haemorrhage

A

metabolic acidosis

51
Q

how could you treat hyperkalemia

A 
calcium resonium (exchanges Ca2+ for K+)
Ca gluconate (reduces excitability of heart, reducing risk of VF)
52
Q

what function of insulin makes it doubly helpful in ketoacidosis and hyperkalaemia

A

it stimulates K+ uptake into cells

53
Q

acid base disorder of vomiting

A

metabolic alkalosis

54
Q

how does vomiting trigger ADH release

A

loss of salt and water –> reduces atrial pressure and carotid sinus pressure –> ADH release

55
Q

how does vomiting trigger renin release

A

loss of salt and water –> hypovolaemia –> carotid sinus pressure reduced

56
Q

how does the kidneys respond to lots of vomiting

A

aldosterone release –> reabsorption of salt and water

ADH –> water reabsorption

57
Q

why is metabolic alkalosis produced by lots of aldosterone

A

because aldosterone reabsorbs Na+ by exchanging it for H+ in the distal tubule, less H+ for HCO3- to join with –> metabolic alkalosis

58
Q

what key things are lost from vomiting

A

water, NaCl and HCl

59
Q

what is the anion gap

A

the difference between the concentration of principal positive and negative ions in plasma

60
Q

what is the purpose of calculating the anion gap

A

it can give more information on the cause of a metabolic acidosis

61
Q

what are the principal cations of plasma

A

Na+ and K+

62
Q

what are the principal anions of plasma

A

Cl- and HCO3-

Urinary - Physiology (10 decks)

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