Pathophys 4.6 Acid Base Physiology

Front 1

intracellular pH is ____

why? (2)

Back 1

about 0.5 pH units lower than extracellular pH

metabolic reactions generate acids

intracellular buffers (proteins and phosphate) defend against this

Front 2

what food groups...?

volatile acid comes from metabolism of _

fixed acid comes from metabolism of _

Back 2

carbohydrates and fats

proteins

Front 3

fixed acids include...

and come from metabolism of...

Back 3

sulfuric acid
--cysteine and methionine
(i.e. sulfur-containing AAs)

hydrochloric acid
--lysine, arginine, histidine
(i.e., positively charged AAs)

Front 4

each day, 288 liters of CO2 is gotten rid of by

(2)

Back 4

body buffers
lungs

Front 5

severe acidemia that develops within minutes of respiratory arrest is caused by

Back 5

accumulation of massive amounts of CO2

Front 6

how much volatile acid

and how much fixed acid

does a 70 kg adult male produce per day?

Back 6

288 liters of CO2 total

70 mmol total
(1 mmol / Kg body weight)

Front 7

extracellular HCO3 is derived from

Back 7

hepatic oxidation of dietary citrate and acetate

Front 8

eating _ affects body pH how?

Back 8

eating citrus fruit alkalinizes the blood and the urine

Front 9

_ is the most important buffer for volatile acid

Back 9

Hemoglobin

Front 10

Hemoglobin is buffer for what?

Back 10

the most important buffer for volatile acid

50% of fixed acids

Front 11

the intracellular buffers include...

the extracellular buffers include...

Back 11

hemoglobin

proteins and phosphates

carbonates and phosphates in bone
- - - - - - - - - - - - - - - - - - -

HCO3-/CO2

Front 12

bone is important for buffering...

Back 12

up to 40% of buffering a fixed acid load

Front 13

how does hemoglobin buffer volatile acid?

(2) concepts

Back 13

1. CO2 can cross cell membranes. so it can easily go into RBCs.


2.
when hemoglobin releases O2 to the tissues,

the pKa of histidine changes

so hemoglobin can bind and buffer more H+

Front 14

high protein diets increase the risk of

(2)

Back 14

osteopenia
calcium oxalate kidney stones

Front 15

chronic metabolic acidosis causes _ because _

Back 15

bone demineralization

Ca++ is leached from bone

Front 16

the most important buffer in the ECF

Back 16

HCO3-/CO2

Front 17

even though HCO3-/CO2 buffer's pKa is 6.1, which is 1.3 pH units less than blood pH, the buffer is effective because...

Back 17

CO2 is regulated independently by the lungs

HCO3- is regulated independently by the kidneys

Front 18

HCO3-/CO2 buffers what?

Back 18

40% of a fixed acid load

completely ineffective for buffering volatile acid (CO2)

Front 19

___ % of filtered HCO3 is reabsorbed

Back 19

99%

Front 20

how much HCO3- is excreted daily in urine?

Back 20

15-20 mmols of HCO3-

Front 21

HCO3- reabsorption mainly happens where?

why?

Back 21

proximal tubules

carbonic anhydrase in the luminal brush border

Front 22

the net result caused by the proximal tubule Na+ H+ exchanger is

Back 22

HCO3- reabsorption

not

H+ secretion

Front 23

how does HCO3- reabsorption happen in the proximal tubules?

Back 23

H+ is secreted by the Na+ H+ exchanger

it combines with filtered HCO3-

carbonic anhydrase catalyzes

--> CO2 + H2O

CO2 diffuses into proximal tubular cell; it and H2O come together

intracellular carbonic anhydrase catalyzes

--> H+ and HCO3-

HCO3- exits cell at basolateral membrane via Na+ HCO3- cotransporter

Front 24

in the distal tubule and collecting ducts there are

three cell types that are responsible for electrolyte reabsorption / secretion

what do they secrete/reabsorb?

Back 24

principal cells
--NaCl reabsorption
--K+ secretion

Type-A intercalated cells
--reabsorb HCO3
--secrete H+

Type-B intercalated cells
--secrete HCO3-

Front 25

how significnat is

reabsorption of HCO3
by Type A intercalated cells?

why?

Back 25

only small amounts

there is no luminal carbonic anhydrase in distal nephron segments

Front 26

HCO3- reabsorption by Type A intercalated cells happens by the action of what ion pumps/channels?

Back 26

H+ ATPase (luminal)
Cl- HCO3- exchanger (basolateral)

Front 27

H+ secretion in type-A intercalated cells happens by the action of

what ion pumps/channels?

Back 27

H+ ATPase is primarily responsible

ATP-dependent H+ K+ exchange also contributes

Front 28

what effect do loops and thiazides have on H+ and K+

Back 28

hypokalemia
alkalemia

(both get reduced in the blood)

Front 29

H+ secreted into urine either causes bicarb reabsorption, OR acid secretion. which one?

the final disposition of H+ secreted into the urine is a function of....

Back 29

the relative concentrations of

bicarb

vs.

titratable acid and NH3

Front 30

the minimum achievable urine pH is _

and is determined by

Back 30

4.5

determined solely by the free H+ concentration

Front 31

most fixed acid is excreted as

Back 31

H2PO4- and NH4+

Front 32

tubular H+ ion secretion mainly takes place where in the nephron?

by what pumps?

Back 32

collecting ducts

H+ ATPase
ATP dependent H+ K+ exchange

Front 33

the most prevalent titratable acid in tubular fluid

Back 33

HPO4 - -

Front 34

if a lab reports "titratable acidity" for a sample of urine, what does that mean?

Back 34

the amount of alkali that must be added to acidic urine

to raise urine pH to 7.40

by titrating H+ ions from the weak acids

Front 35

_ is not a titratable acid. why?

Back 35

NH4+

its pKa is 9.3

(which means that at pH of 9.3, half of it is NH3, half is NH4+. At a pH of 7.40, most of it will still be NH4+ -- hardly any H+ will be given up until the titration goes further, to a higher pH.)

Front 36

titratable acidity

regulation

therefore...

Back 36

it's hardly regulated.

titratable acidity accounts for a constant excretion of 36 mmols of fixed acid daily

Front 37

_ is the most important mechanism the kidney has, to regulate fixed acid excretion

Back 37

NH4+ secretion into the proximal tubules

Front 38

two advantages NH4+ has over H2PO4-, for acid secretion

Back 38

NH4+:

unlimited source (from amino acids)

much higher pKa (9.3)

vs. H2PO4-

limited by how much of it is filtered at the glomerulus

pKa 6.8

Front 39

the vast majority of NH4+ is made

where?

from what?

Back 39

in proximal cells

from glutamine

Front 40

two ways that NH4+ gets into the urine

where

Back 40

Na+ NH4+ exchanger

(at lumen of proximal tubules)


NH3 diffuses into the urine and combines with H+

(from interstitum and blood; at the level of the collecting tubules/ducts)

Front 41

daily net acid excretion =

Back 41

NH4+ + H2PO4- - HCO3-

in the urine

Front 42

list 6 things that cause

urinary H+ excretion

Back 42

the two most important:

increase in PaCO2
increase in plasma H+


decrease in plasma volume
hyperaldosteronism

chloride loss
hypokalemia

Front 43

what three electrolyte disturbances can increase urinary H+ excretion?

Back 43

increased plasma H+
(decreased pH)

low Cl-
low K+

Front 44

how does diabetic ketoacidosis affect titratable acid levels in the urine?

why?

Back 44

it increases it

- - - - - - - - - - - - -
gist: this ketoacid below has a pKa < 7.40 and is therefore a titratable acid.

[large amounts of beta-hydroxybutyrate (pKa = 4.8) appear in the urine. as OH- is added to bring the urine up to 7.40, this weak acid gives up H+ ions in the titration.]