Jan10 M1-Acid Base Physiology Flashcards

1
Q

lower and upper limit of pH before death

A

6.8 to 8.0

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2
Q

pH formula

A

-(log H+)

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3
Q

blood pH formula

A

6.1 + log (bicarb/0.03PCO2) = pH

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4
Q

3 values to check for acid base balance

A

pH, CO2, bicarb

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5
Q

rule in HCO3 and CO2 variation

A

always move in the same direction, no matter which one is the primary problem

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6
Q

how to know if problem is primarily respiratory or metabolic

A

if pH and CO2 change in same direction, metabolic

if pH and CO2 change in opposite direction, respiratory

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7
Q

how much CO2 prod daily and how

A

15000 mmol. because of the Krebs cycle

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8
Q

2 types of acids in the body and what they correspond to

A
carbonic acid (volatile): CO2
non-carbonic acid (non-volatile): lactic, phosphoric, sulfuric
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9
Q

non-carbonic acids source and how much produced daily

A

from a.a metabolism. 50-100 mmol

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10
Q

buffer def

A

any substance that can reversibly bind H+ ions

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11
Q

how H+ ions are buffered in the body

A

by extracellular (HCO3, etc.) and intracellular buffers

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12
Q

major intracellular buffers

A

phosphates, proteins and carbonate (CO3) in bone

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13
Q

2 steps to acid metabolism in the body

A
  1. buffering

2. excretion

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14
Q

how much acid do the kidneys and the lungs excrete daily

A

lungs: 15000mmol
kidneys: 50-100 mmol

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15
Q

in the kidney, excreting acid is the equivalent of what

A

generating bicarb (50-100 mmol daily)

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16
Q

minimal tubular pH and what takes care of buffering there

A

4.5

ammonium (NH4+) and hydrogen phosphate (HPO4 2-)

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17
Q

where are acids handled in the tubules

A

PCT, loop of Henle, CD

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18
Q

main thing kidney does to keep the serum bicarb

A

reabso of filtered bicarb

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19
Q

how is bicarb reabsorbed at the tubules (PCT)

A
  1. H+ pumped out via Na-H exchanger
  2. H+ and bicarb form CO2 (via luminal CA)
  3. CO2 enters membrane and becomes H+ and bicarb via cellular CA
  4. bicarb in blood via Na-3bicarb cotransporter
  5. H+ out again
20
Q

CA inhibitors inhibit what CAs and consequence on urine, what is excreted

A

CA in and out of the cell inhibited. No more H+ made so Na-H exchanger stops working. Pee NaHCO3

21
Q

CAi used for what (2)

A

glaucoma and mountain sickness

22
Q

principle of using CA in mountain sickness

A

you hyperventilate because of the hypoxia so lose a lot of CO2, become alkalotic. CA stops that by inhibiting PCT reabso of bicarb

23
Q

can you induce alkalosis by ingesting too much bicarb?

A

no, excess filtered at kidney is excreted

24
Q

2 ways for the kidney to generate new bicarb and why must do that

A
  1. urine buffering by H-HPO4 adds 1 bicarb to plasma
  2. urine buffering by ammonium adds 1 bicarb to the plasma
    * necessary bc need NEW bicarb to buffer the NEW acid. (good to reabso bicarb but need new)
25
Q

when does the kidney start to use H-HPO4 urine buffering (one method to make new bicarb)

A

when there is no more bicarb available in the tubule and all has been reabso

26
Q

Urine buffering by H-HPO4: how it works to generate a bicarb

A

CA in the cell makes H+ and HCO3- from H2O and CO2. H+ out to bind HPO4 and form H2PO4. bicarb in

27
Q

Urine buffering by ammonium: how it works to add 1 bicarb to the plasma

A
  1. glut reabso at PCT via Na-a.a cotransporter
  2. glut forms NH4+ + bicarb and bicarb taken in
  3. NH4+ out via Na-H exchanger (takes H+’s spot)
28
Q

main adaptive response to an acid load and how much bicarb it produces daily

A

NH4+ excretion. makes 30-40 mmol daily

29
Q

other way to secrete NH4+ coming from glutamine than Na-H cotransporter

A

NH3 in the cell diffuses in the lumen and binds an H+ to make ammonium

30
Q

other place in the tubule where there is acid handling and what mechanism is used

A

loop of Henle. 1st mech for new bicarb. H2O and CO2 make HCO3 and H+ via CA. HCO3 in via Na-HCO3 cotransporter. H+ out via Na-H exchanger

31
Q

what is the main determinant of acid excretion and how it works (acts on what)

A

low extracellular pH acts on 2 mech for new bicarb bc low pH = acid load

  • revs up Na-H antiporter in PCT
  • increases glut uptake and metab by PCT
  • revs up Na-3 bicarb cotransporter in PCT
  • revs up H-K activity in CD (alpha-int)
  • promotes ammonium excretion
32
Q

H+ handling in the CD (2 things)

A
  1. alpha-int cells have H+ (out) K (in) exchanger ATPase (and then bicarb-Cl exchanger)
  2. NH3 that diffused out into the tubule lumen becomes NH4+ bc of that acid and goes out
33
Q

how to maintain acid base balance in renal failure

A

IV D5W + bicarb (hypertonic but sugar quickly metab)

34
Q

normal arterial and venous pH, H+, CO2 and bicarb values

A

arterial: 7.4, 40, 40, 24
venous: 7.45, 45, 45, 25

35
Q

causes of metabolic acidosis

A

diarrhea (loss of bicarb), renal failure, poisoning, diabetic ketoacidosis, lactic acidosis

36
Q

2 responses to metabolic acidosis

A
  1. buffering by IC and EC buffers

2. compensatory rise in ventilation

37
Q

2 causes of metabolic alkalosis

A

vomiting, hyperaldo (increased H secretion in DCT and CCD bc revs up H-K ATPase in alpha int)

38
Q

2 causes of respiratory acidosis

A

acute respiratory failure (morphine)

COPD (chronic)

39
Q

compensation to metabolic alkalosis

A

less bicarb reabso

40
Q

compensation to resp acidosis

A

kidney increases acid (mostly NH4+ excretion)

41
Q

4 causes of resp alkalosis

A

pneumonia, anxiety, pregnancy, mountaineering

42
Q

why pregnancy causes resp alkalosis

A

medulla stimulated at lower CO2 (stimulates breathing at lower CO2)

43
Q

contraction alkalosis def

A

volume contraction state where all bicarb is retained

44
Q

ions left and ions reabsorbed in contraction alkalosis + their urine amount

A

Na and bicarb all reabsorbed (PCT important)

Cl low in serum and low in urine bc is lost in the fluid loss

45
Q

why can’t excrete bicarb in contraction alkalosis

A

because Na reabsorbed at PCT so bicarb too. if euvolemic, less Na-H exchanger work so more H left in the cell and unavailable to bind bicarb in urine to make it enter the PCT so bicarb stays in the urine

46
Q

how to treat contraction alkalosis

A

give NS so that Na not too retained anymore