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PBL SEM 4 > acid-base balance and the kidney > Flashcards

acid-base balance and the kidney Flashcards

1
Q

pH equation

A

-log10[H+]

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2
Q

normal pH of arterial blood

A

7.4

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3
Q

what is pH regulation dominated by?

A

HCO3-/CO2 buffering system

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4
Q

what is the henderson-hasselbalch equation?

A
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5
Q

what causes a resp acidosis/alkalosis?

A

acidosis = inceasesd CO2 eg poor gas exchange in lungs
alkalosis = decreased CO2 eg hyperventilation

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6
Q

what causes a metabolic acidosis/alkalosis?

A
  • acidosis = decreases HCO3-
  • alkalosis = increased HCO3- = RARE
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7
Q

what is normal HCO3- is mM?

A

24 mM

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8
Q

what is normal CO2 in mM?

A

1.2 mM = 40mmHg

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9
Q

how many mmol of CO2 is produced a day?

A

15 000

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10
Q

metabolism produced __ mmol H+ a day

A

40
— non-volatile acids = sulphyric, phosphoric, organic acids

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11
Q

net uptake of __mmol H+ a day by GIT

A

30

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12
Q

kidney has to excrete __mmol H+ a day and reabsorb all the filtered ____ (equivalent to 4000 mmol H+ a day)

A
  • 70
  • HCO3-
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13
Q

typical urine output a day

A

1.5 litres

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14
Q

what are the 3 mechanism of acid-base balance in the kidney?

A
  1. reabsorption of filtered bicarbonate
  2. excretion of H+ as titration acid
  3. excretion of H+ as NH4+ (ammonium)
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15
Q

describe reabsorption of filtered HCO3-

A
  • H+ secretion at apical membrane reclaims HCO3- as Co2 + H2O
  • HCO3- extruded at basolateral membrane
  • net transfer of HCO3- from lumen to blood
  • involves carbonic anhydrase was II and IV
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16
Q

carbonic anhydrase II vs IV

A

II = intracellular in cytoplasm
IV = expressed in apical membrane

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17
Q

describe excretion of H+ as ‘titratable acid’ TA

A
  • H+ and HCO3- generated from CO2 and H20 in cell
  • secreted H+ is mostly buffered by filtered phosphate - also creatinine, urate etc
  • new HCO3- enters circulation and neutralises acidity
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18
Q

describe excretion of H+ as NH4+ (ammonium)

A
  • NH4+ synthesised by the kidney
  • comes from glutamine metabolism
  • new HCo3- enters circulation and neutralises acidity
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19
Q

what are the sites of HCO3- reabsorption?

A
  • most is reabsorbed in the PCT
  • small amounts in TAL (10%), DCT (6%) and CD (4%)
  • very little excreted : <0.01%
20
Q

where is most of the NH4+ secreted?

A

PCT

21
Q

what mmol of acid are excreted by kidneys?

A

70mmol

= 40mmol NH4+ + 30mmol TA

22
Q

kidneys excrete additional H+ as what?

A
  • titratable acid using filtered buffers like phosphate
  • NH4+ = synthesised
23
Q

when does renal tubule acidosis occur and what are the different types?

A
  • occurs when there are defects in HCO3- reabsorption and H+ excretion

4 types:
- 1 = distal RTA
- 2 = proximal RTA
- 3 = mixed (1+2)
- 4 = hyperkalaemia RTA (hypoaldosteronism)

24
Q

what is the dominant transporter in the PCT?

A

NHE3

25
Q

what predominates later in the tubule?

A

H+ ATPase

26
Q

in the PCT, HCO3- in tubular fluid is converted to CO2 and OH- as a result of what? what happens to the products?

A

carbonic anhydrase IV

  • CO2 diffuses into cell and combines with OH- (via CA II) to form HCO3-
  • OH- combines with H+ in tubular fluid to form water — diffuses into cell via osmosis, then breaks down into H+ and OH-
27
Q

in the PCT, how does HCO3- leave the cell on the basolateral side?

A

kNBCe1

28
Q

describe kNMCe1

A
  • how HCO3- crosses basolateral membrane in early PCT
  • electrogenic with a net transport of 2 -ve charges
  • 1 Na+ for every 3 HCO3-
  • membrane potential helps drive HCO3- exit
29
Q

NHE3 vs H+ ATPase gradient

A
  • NHE3 = large capacity but limited gradient
  • H+ ATPase = can generate a larger capacity
30
Q

what transporters are present in the apical membrane of the TAL and DCT?

A

same as PCT

NHE3 and H+ ATPase

31
Q

what is used instead of kNBCe1 on the basolateral side of the cell for HCO3- reabsorption in TAL and DT?

A

AE2 = HCO3-/Cl- exchanger

32
Q

where is the majority of the V-type H+ ATPase activity?

A

later on in tubule — a-intercalated cells of collecting tubule and duct cells

33
Q

what is the main function of the H+/K+ ATPase in the a-intercalated cells of the CD?

A

K+ reabsorption

34
Q

what is on the basolateral membrane to reabsorb HCO3- in the a-intercalated cells?

A

kAE1 (HCO3- Cl- exchanger)

35
Q

where are the V-type H+ ATPase cells in the collecting dyct?

A

apical membrnae of a-intercalated cells — NOT on principal cells

36
Q

where and how is NH4+ produced?

A

by glutamine metabolism in PCT

37
Q

NH4+ is secreted as ____ which passively diffuses across ___ membrane. NH4+ then reformed by combining with __ (which is excreted in exchange for __)

A
  • NH3
  • apical
  • H+
  • Na+
38
Q

what does glutamine metabolism produce?

A

NH4+ and OH-

39
Q

what happens to the OH- produced in glutamine metabolism in the PCT?

A

combine with CO2 via CA II to form HCO3- — this can then enter blood across basolateral membrane via NMB

40
Q

what happens to NH4+ in the TAL?

A
  • reabsorbed via ROMK2 chanel and NKCC1 (NH4+ in oak e of usual K+_
  • low permeability at apical membrane, so it leaves across basolateral membrane
41
Q

what happens to NH4+ in the collecting duct?

A
  • re-secreted
  • most crosses epithelium as NH3 (can freely diffuse across membrane)
  • maybe some NH4+ carried by NaK ATPase
42
Q

describe type 1 — distal renal tubular acidosis

A
  • defective H+ excretion by distal segment of nephron
  • inability to acidify urine — serious systemic consequences = metabolic acidosis
  • may be incomplete — compensatory mechansims of PCT
  • but treatable by HCO3- supplementation
  • several transproter mutiatons — mainly affected the a-intercalated cells : kAE1, V-type H+ ATPase, CAII (proximal affects too)
43
Q

describe type 2 — proximal RTA

A
  • rare autosomal recessive disease
  • impaired HCO3- reabsorption in PCT
  • severe metabolic acidosis
  • not treatable by HCO3- supplementation (80% f bicarbonate is reabsorbed in PCT)
  • attributed to mutations in kNBCe1
  • ocular abnormalities too because of kNMCe1 and pNBCe1 expression there too
44
Q

resp/metaoblic acidosis :

an increase in PCO2 (resp) or decrease in HCO3- btoh directly stimulate what?

A

an increase in H+ secretion and increase in NH4+ synthesis by proximal tubule

45
Q

chronic resp/metabolic acidosis leads to an increased expression of what?

A

NHE3 and kNMCe1

46
Q

resp/metabolic alkalosis — chronic leads to more what?

A

more B-intercalated cells (HCO3- secreting) in collecting tubule

47
Q
A

PBL SEM 4 (50 decks)

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