l12 acid base Flashcards

1
Q

how many m moles of CO2 produced from metabolism

A

20,000 m moles

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2
Q

what are volatile and non volatile acids

A

volatile acids are H2CO2 and CO2, fixed acids are nonvolatile acids (H+ A-)

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3
Q

how many m moles of fixed acids are produced daily

A

60 m moles

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4
Q

how much filtered HCO3 must be reabsorbed to maintain acid-base balance

A

4300 meq (24 meq/L X 180 L/day)

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5
Q

how much HCO3- needs to be produced per day

A

60 meq

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6
Q

what is the dominant H+ mechanism of transport in proximal and distal tubule?

A
  • proximal: NHE3 in prosimal (depends on Na-K ATPase basolateral)
  • distal/cd: H+ active pump on apical membrane, lowers pH of luminal fluid below proximal tubule
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7
Q

draw bicarbonate reabsorption in proximal tubule

A

should have:

apical: co2 diffusing in, H+ moving out by Na/H exchanger or ATPase
basolateral: HCO3- moving out with Na and 3Na out:2K in

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8
Q

what are the two urinary buffers of h+

A

phosphate (in luminal fluid) and ammonia (in proximal tubule cells, derived from metab of glutamine/amino acids)

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9
Q

what is titratable acidity

A

all buffers in urine with pk around urine pH, most importantly phosphates NOT NH4

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10
Q

how much of the urine acid is accounted for by titratable acids

A

1/3 of titratable acids account for urine acidity

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11
Q

whend does endogenous production of filterable buffer/titratable acids increase?

A

in diabetes with production of ketoacids

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12
Q

how is nh4 transported

A

in proximal tubule: via NH4/Na exchange into lumen
TAL: reabsorbed by substituting on Na/2Cl/K co transporter and is in equilibrium with NH3 in interstitium
cd: Rh glycoproteins transport NH3 and H into fluid where NH4 is trapped and maintains interstitial gradient

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13
Q

what hormones and transporters are stimulated by acidosis

A
  • ET1 transporter in pt cells increase NHE3 NBCe1 transporters
  • cortisol from adrenal cortex increase NHE3 NBCe1 transporters
  • PTH- inhibits phosphate reabsorption in PT so it can be used as T.A
  • increase NHE3 Rh glycoproteins and H ATPAse in acute response
  • increase proteins ammoniagenesis for chronic response
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14
Q

Primary disturbance of respiratory acidosis, what is the effect on plasma k (hypo or hyper-kalemia)?

A

Respiratory disturbance won’t normally affect k, if anything H moves into cells and K moves out of cells and increases plasma K (hyperkalemia)

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15
Q

Metabolic alkalosis has what effect on plasma K

A

Movement of H out of cells promotes K uptake into cells and causes hypolalemi

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16
Q

Example of metabolic acidosis

A

Diarrhea causes loss of HCO3-from body and thus decrease in buffering.

17
Q

Calculate total H secreted

A

Total h = reabsorbed HCO3- + new HCO3-
reabsorbed HCO3- = filtered HCO3- - lost urine

NEW HCO3- secretes H into urine= TA + NH4+

18
Q

Diarrhea

  • what is the composition of diarrhea fluid
  • what is hr and bp
  • hyper or hypo ventilating
  • is hematocrit high or low
  • what is plasma Na, Cl-, K, HCO3-, and Cre
A

Diarrhea fluid is isosmotic, alkaline (lots of HCO3-), high in K

  • bp is low and hr is fast - sympathetics
  • high hematocrit because losing fluid from ECF
  • hyperventilating to breathe off CO2 to lowed pH
  • diarrhea is metabolic acidosis with respiratory compensation
  • plasma Na no change because losing isosmotic fluid, [Cl-] is high to balance loss of HCO3-, hypo kalemia (H in, K out, and K secreted due to high tubular flow), HCO3- low because loss
  • Cre is high in plasma because GFR is low