Guyton Ch30 Regulation Oa Acid Base Balance

Front 1

How do you calculate the amount of CO2 in the blood?

Back 1

the amount of CO2 in the blood is a linear function of PCO2 times the solubility coefficient for CO2;
α = 0.03mmol/mmHg

So, CO2 = pCO2*α

Front 2

H-H eqn:
pH = pK + ?

Back 2

log(bicarb/CO2)


CO2 = pCO2*0.03

Front 3

What's pK of bicarb

Back 3

6.1

Front 4

Where does the phosphate buffer system work most and best?

Back 4

in the renal tubules and intracellularly

Front 5

What is the pK of the phosphate buffer system?

Back 5

6.8

Front 6

Diffusion of H+ and bicarb into cells is very slow except what cells?

Back 6

RBCs

Front 7

the kidneys regulate extracellular fluid H+ concentration through three fundamental mechanisms:

Back 7

(1) secretion of H+, (2) reabsorption of filtered HCO3-, and (3) production of new HCO3-

Front 8

Where in the tubular epithelium is H+ secreted by primary active transport?

Back 8

Beginning in the late distal tubules and continuing through the remainder of the tubular system,

INTERCALATED CELLS!

Front 9

How does bicarb get out of the proximal tubule epithelium and into the intersitium?

Back 9

Na+-bicarb cotransport and


Cl--bicarb exchange

Front 10

Where in the nephron is H+ secreted by secondary active transport?

Back 10

proximal tubule, loop of Henle, and early distal tubule.

Front 11

What counter-transport does H+ use to get in to the proximal tubule lumen?

Back 11

H+-Na+ exchange

(using energy from Na+ gradient created by Na+-K+ ATPase on basolateral side)

Front 12

Why is Cl- leaking into the lumen at intercalated cells

Back 12

From the late distal tubule,
Bicarb gets to the interstitium using a Cl--bicarb exchanger

Front 13

80 mEq of non-volatile acid must be excreted/day. How much urine volume must be used if only free H+ is used to excrete the acid.

Back 13

2667 L

Front 14

How does the extracellular fluid get new bicarb?

Back 14

When secreted H+ combines with HPO4-- or NH3 or other buffer than bicarb

Front 15

Which is more important quantitatively, the phosphate buffer system or the ammonia buffer system?

Back 15

ammonia

Front 16

For each glutamine metabolized by the proximal tubules, how many NH4+ go into the lumen?

Back 16

2


(and 2 new bicarbonates are absorbed into the ECF)

Front 17

How does NH4+ get into the lumen of the proximal tubule?

Back 17

NH4+/Na+ counterport

Front 18

In the collecting tubules, NH3 can freely cross into the lumen. If an NH3 grabs an H+, what happens?

Back 18

It gets excreted.

Front 19

For every NH4+ excreted, how many new bicarb are added to the ECF?

Back 19

1

Front 20

Which buffer system provides 50% of acid excretion in normal conditions

Back 20

ammonium-ammonia

Front 21

Which buffer system is dominant in the setting of chronic acidosis?

Back 21

ammonium-ammonia

Front 22

How do you calculate net acid excretion?

Back 22

NH4+ excretion
+
other buffer excretion
-
bicarb excretion

Front 23

What is "other buffer excretion" determined by?

Back 23

titratable acid

found by titrating urine with NaOH to pH of 7.4

Front 24

The net acid excretion must equal the net addition of what into the blood?

Back 24

bicarb

Front 25

The most important stimuli for increasing H+ secretion by the tubules in acidosis are

Back 25

(1) an increase in PCO2 of the extracellular fluid and
(2) an increase in H+ concentration of the extracellular fluid (decreased pH).

Front 26

Aldosterone stimulates the secretion of H+ by what part of the nephron

Back 26

the intercalated cells of the collecting duct.

Front 27

Some causes of renal tubular acidosis include chronic renal failure, insufficient aldosterone secretion (______ disease), and several hereditary and acquired disorders that impair tubular function, such as _____ syndrome.

Back 27

Addison’s



Fanconi’s

Front 28

________ is probably the most frequent cause of metabolic acidosis

Back 28

Severe diarrhea

Front 29

How might vomiting cause metabolic acidosis (it usually causes metabolic alkalosis)

Back 29

if the vomit comes from deep in the GI tract so that bicarb is lost

Front 30

what acid causes diabetic metabolic acidosis

Back 30

acetoacetic acid,

Front 31

acidic poisons that can cause metabolic acidosis

Back 31

acetylsalicylics (aspirin)
methanol (--> metabolized to formic acid)

Front 32

administration of diuretics (except which kind?) may cause alkalosis

Back 32

carbonic anhydrase inhibitors

Front 33

Why are sodium lactate and sodium gluconate given IV to treat acidosis?

Back 33

because of the potentially dangerous physiologic effects of IV bicarb treatment,

Front 34

treatment of alkalosis

Back 34

ammonium chloride po


(in liver, urea and HCl are formed)

Front 35

acid-base nomogram:

If your values are in the shaded part, what do you have?

Back 35

simple acid-base disturbance


(if not, it's "mixed", like the emphysema pt with diarrhea)

Front 36

Why would the anion gap increase?

Back 36

if unmeasured anions rise

or

if unmeasured cations fall

Front 37

If plasma Cl- increases in proportion to the fall in plasma HCO3-, the anion gap will remain normal, and this is often referred to as ______ metabolic acidosis.

Back 37

hyperchloremic

Front 38

Metabolic acidosis conditions associated with a normal anion gap

Back 38

diarrhea
renal tubular acidosis
carbonic anhydrase inhibitors
Addison's disease

Front 39

Metabolic acidosis conditions associated with an increased anion gap

Back 39

DM
lactic acidosis
chronic renal failure
aspirin poisoning
methanol poisoning
ethylene glycol poisoning
starvation