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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
true/false NH4+ formed in cell can be pumped out into lumen by exchanging with Na+
true
26
where is ammonium ion mostly formed (i.e. combined with H+) in the proximal tubule
in the cell, it is then pumped into lumen by exchanging with Na+
27
where is ammonium ion mostly formed (i.e. combined with H+) in the distal tubule
in the lumen
28
effect of high intracellular pH on renal glutaminase
reduced renal glutaminase activity
29
effect of low intracellular pH on renal glutaminase
increased renal glutaminase activity, to excrete the increased H+
30
what is the main adaptive response of the kidneys in response to acidosis
to increase NH4+ production through renal glutaminase and excrete more H+
31
how long does it take for the kidneys to have their maximal effect in response to acidosis
4-5 days
32
why does it take the kidneys so long to compensate for acidosis/alkalosis
because of the requirements of the increase in protein synthesis/switch off the ability to make NH4+
33
how much H+ can be excreted at maximum in acidosis per day
250mmoles/L
34
causes of respiratory acidosis
drugs - barbituates, opiates | other - obstruction, empysema, asthma, bronchitis
35
effect of PCO2 on HCO3- reabsorption
increases ability to reabsorb
36
effect of hyperventilation on pCO2
reduces it --> increased ventilation blowing off more CO2
37
causes of respiratory alkalosis
hyperventilation, aspirin, high altitude
38
how does high altitude affect blood pH
at high altitudes the low O2 stimulates peripheral chemoreceptors to increase ventilation. More CO2 is blown off meaning less H+ --> alkalosis
39
origin of a metabolic acidosis
reduced HCO3- conc
40
causes of metabolic acidosis
increased H+ production (ketoacidosis), failure to excrete H+, loss of HCO3- in diarrhoea
41
process of metabolic acidosis
reduced HCO3- --> increased H+ --> stimulation of ventilation --> blow off CO2 --> less H+ made
42
renal response to metabolic acidosis
takes some time to increase H+ excretion and generate new HCO3-
43
true/false in metabolic acidosis/alkalosis respiratory compensation delays renal correctionbut protects the pH
true
44
origin of metabolic alkalosis
increase in HCO3-
45
causes of metabolic alkalosis
vomiting (h+ loss), excess H+ excretion (aldosterone and liquorice), blood transfusions
46
how do blood transfusions cause metabolic alkalosis
the anticoagulant citrate converts to bicarbonate
47
acid base disorder of ketoacidosis
metabolic acidosis
48
acid base disorder of bronchitis
chronic respiratory acidosis
49
what is the risk from hyperkalaemia
ventricular fibrillation
50
acid base disorder of haemorrhage
metabolic acidosis
51
how could you treat hyperkalemia
``` calcium resonium (exchanges Ca2+ for K+) Ca gluconate (reduces excitability of heart, reducing risk of VF) ```
52
what function of insulin makes it doubly helpful in ketoacidosis and hyperkalaemia
it stimulates K+ uptake into cells
53
acid base disorder of vomiting
metabolic alkalosis
54
how does vomiting trigger ADH release
loss of salt and water --> reduces atrial pressure and carotid sinus pressure --> ADH release
55
how does vomiting trigger renin release
loss of salt and water --> hypovolaemia --> carotid sinus pressure reduced
56
how does the kidneys respond to lots of vomiting
aldosterone release --> reabsorption of salt and water | ADH --> water reabsorption
57
why is metabolic alkalosis produced by lots of aldosterone
because aldosterone reabsorbs Na+ by exchanging it for H+ in the distal tubule, less H+ for HCO3- to join with --> metabolic alkalosis
58
what key things are lost from vomiting
water, NaCl and HCl
59
what is the anion gap
the difference between the concentration of principal positive and negative ions in plasma
60
what is the purpose of calculating the anion gap
it can give more information on the cause of a metabolic acidosis
61
what are the principal cations of plasma
Na+ and K+
62
what are the principal anions of plasma
Cl- and HCO3-

Urinary - Physiology (10 decks)

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