Acid Base Phys Review

Front 1

Normal range of pH

Back 1

7.35 - 7.45

Front 2

A) pH in acidemia
B) pH in alkalemia

Back 2

A) less than 7.35
B) greater than 7.45

Front 3

Range of pH compatible with life

Back 3

6.8-8

Front 4

What is volatile acid?

Back 4

CO2

Front 5

Where does volatile acid come from?

Back 5

oxidative metabolism

Front 6

CO2 + H20 -->

Back 6

H2CO3 --> H+ + HCO3-

Front 7

Where is CO2 converted to H+ and HCO3-?

Back 7

RBCs

Front 8

What happens once CO2 converted to H+ and HCO3- in RBCs?

Back 8

H+ remains in red cell and is buffered by deoxyHb; HCO3- moves into plasma in exchange for Cl-

Front 9

What happens to CO2 in lungs?

Back 9

Reaction moves in reverse and CO2 is xpired

Front 10

sulfuric and phosphoric acids are what type of acid?

Back 10

fixed

Front 11

How are fixed acids eliminated?

Back 11

Must be buffered and excreted by kidneys

Front 12

Henderson - Hasselbalch eqn

Back 12

pH = pK' + log [HA/A-]

Remember protonated / unprotonated

Front 13

How to convert PCO2 in mmHg to [CO2] for HH eqn

Back 13

multiple by 0.03

Front 14

HH eqn for HCO3-/CO2 buffer pair

Back 14

pH = pK + log [HCO3-/(0.03 * P_CO₂)

Front 15

Contents of a buffered soln

Back 15

Weak acid and conjugate base (or weak base and conjugate acid) that resists change in pH

Front 16

When does best buffering occur?

Back 16

Within 1.0 pH unit of the pK, in the linear range of titration curve, because both forms of buffer are present.

That is, if H+ is added, some A- will get converted to HA

Front 17

Major extracellular buffer

Back 17

HCO3-/CO2

Front 18

What happens if H+ is added to ECF?

Back 18

It combines with HCO3 to form H2CO3.

The H2CO3 is converted to CO2 and H20. The CO2 is excreted by lungs.

Front 19

HPO4^2-/H2PO4- is a buffer important where?

Back 19

urinary

Front 20

Where are there symptoms of hypocalcemia in acute respiratory alkalosis?

Back 20

There is competition between Ca2+ and H+ for plasma protein binding sites.

Where there's not enough H+ (like in hyperventilation), thus more Ca2+ binds to plasma proteins like albumin.

Front 21

What are the intracellular buffers?

Back 21

1) Organic phosphates
2) Proteins like Hb

Particularly important are imidazole and α amino gruops due to ideal pKs

Front 22

H+ can switch with ___

Back 22

K+

Front 23

Acidemia produces ____kalemia and alkalemia produces ____kalemia.

Back 23

hyper; hypo

Front 24

What is lactic acidosis?

Back 24

When lactate, and organic anion, moves with H+.

Front 25

What are kidneys responsible for in normal acid-base balance?

Back 25

1) Reabsorption of filtered bicarb
2) Excretion of H+ as titratable acid and NH4+ which is accompanied by reabsorption of new bicarb

Front 26

How is H+ secreted from cell to lumen in kidney?

Back 26

Via a Na+-H+ exchanger.

Front 27

How is H+ used to reabsorb filtered HCO3?

Back 27

1) H+ secreted from cell to lumen via Na+/H+ exchanger.

2) In the lumen, H+ combines with filtered HCO3 to form H2Co3.

3) Then luminal carbonic anhydrase converts to CO2 and H20, which enters cell and then dissociates into H+ and HCO3-.

4) The HCO3 is reabsorbed into bloodstream, and the H+ is recycled by getting secreted via the Na/H exchanger to continue participation.

Front 28

What do carbonic anhydrase inhibitors do in tubular lumen?

Back 28

Inhibit reabsorption of filtered HCO3, but it's required to be in CO2+H2O form to get reabsorbed.

Front 29

T/F The reabsorbed HCO3- was originally in the glomerular filtrate

Back 29

T

Front 30

T/F No net H+ is secreted

Back 30

T. The H+ is recycled across luminal membrane.

Front 31

How does the kidney regulate HCO3- when there is metabolic alkalosis (too much HCO3- in blood?)

Back 31

Not all of the HCO3- that is filtered will get reabsorped because there is a max capacity.


This is exactly what is needed - to excrete excess bicarb.

Front 32

What is source of H+ secreted for the reabsorption of filtered HCO3-?

Back 32

Comes from intracellular CO2.

Therefore, changes in arterial P_CO2 produce changes in intracellular CO2 and alter reabsorption of filtered HCO3-

Front 33

What is the basis for renal compensation for respiratory acid-base disorders?

Back 33

changes in arterial PCO2 produce changes in intracellular CO2 and alter reabsorption of filtered HCO3-.

1) In respiratory alkalosis, there is decreased CO2, therefore decreased H+ for bicarb reabsorption, so more bicarb gets excreted.

2) In respiratory acidosis, there is increased H+ due to increased CO2, so more HCO3- that is filtered gets reabsorbed.

Front 34

Volume contraction (increases, decreases) bicarb reabsorption while volume expansion (increases, decreases) bicarb reabsorption.


Why?

Back 34

increases; decreases.


Due to starling forces. In volume contraction, oncotic pressure of blood is higher so it pulls more fluid out and bicarb comes with

Front 35

What does angiotensin II directly stimulate wrt acid/base?

Back 35

1) Na+-H+ exchange (H+ out, Na+ in)

2) HCO3- reabsorption

Front 36

What is contraction alkalosis?

Back 36

In volume contraction, RAA system is activated.

Stimulates reabsorption of bicarb --> increased plasma bicarb concentration.

Increased aldosterone stimulates H+ secretion and new HCO3- reabsorption in distal tubule. Increased HCO3- reabsorption also increases HCO3- concentration in blood.

Front 37

What pump is stimulated by aldosterone?

Back 37

The H+ ATPase in α intercalated cells of distal tubule and collecting duct.

H+ gets secreted into lumen.

Front 38

How is H+ excreted as titratable acid?

Back 38

1) H+ secreted into lumen by H+ ATPase in α intercalated cells of distal tubule and collecting duct.

2) H+ combines with urinary buffers, primarily HPO4^2-.

3) HPO4^2- is converted to H2PO4- which is excreted in urine (this is the titratable acid).

4) The secreted H+ comes from CO2 and H20 in the cell that combine to form H2CO3 that dissociates into H+ (which is secreted and excreted) and HCO3- (reabsorbed, "new")

The importance of this is to replace bicarb that had been previously consumed in buffering fixed acids produced from protein catabolism.

Front 39

What is minimum urine pH?

Back 39

4.4. After this, H+ secretion will no longer occur.

Front 40

What happens as [HPO4^2-] in tubular fluid increases?

Back 40

There is more available to combine with H+, and the greater excretion of H+ as titrable acid because the buffer keeps urine pH >4.4.

Front 41

How is NH3 also used as a way to excrete fixed acid and absorb new bicarb?

Back 41

1) NH3 is highly lipid-soluble and diffuses into lumen

2) Secreted H+ combines with NH3 --> NH4+

3) NH4+ is an ion and NOT lipid soluble. It is trapped in the lumen (diffusion trapping) and excreted.

4) The secreted H+ came from cellular CO2.

Newly made HCO is reabsorbed into blood to replace bicarb previously consumed in buffering fixed acids.

Front 42

How does decreased urinary pH affect NH3 combination with H+ to form NH4+?

Back 42

1) Decreased urinary pH favors the formation of NH

2) Presence of NH creates favorable concentration gradient for NH3 to continue diffusing into lumen.

3) The more NH3 that is present in the lumen, the more H+ that can combine with it

4) Therefore the more NH4+ formed and excreted.

Helpful in acidosis.

Front 43

Adaptive increase in ammonia production in acidosis is a major mechanism to increase H+ excretion EXCEPT in what case?

Back 43

When the loss of renal tissue in Chronic renal failure and resulting inability to make NH3 is CAUSE of metabolic acidosis.

Front 44

_____kalamia inhibits NH3 synthesis and decreases excretion of H+ as NH4+

Back 44

Hyper

Front 45

Caused by overproduction of fixed acid OR loss of base

Back 45

Metabolic acidosis

Front 46

What is respiratory compensation for metabolic acidosis?

Back 46

1) Start with too much acid.

2) Bicarb is consumed in buffering the excess H+.

3) pH decreases.

4) Decreased pH <b>stimulates breathing to get rid of CO2</b>, therefore P_CO2 is below normal.

Front 47

In respiratory compensation for metabolic acidosis, there will be (hyper/hypo)ventilation

Back 47

HYPER. Trying to get rid of excess acid, so Pco2 will decrease.

Front 48

Chronic metabolic acidosis (except in renal failure) is associated with increased in what?

Back 48

NH3 synthesis

Front 49

Results from loss of fixed H+ from body (eg. from vomiting) or from gain of base.

Back 49

Metabolic alkalosis

Front 50

What is respiratory compensation for metabolic alkalosis?

Back 50

1) Start with not enough acid/too much base.

2) Breathing slows (hypoventilation)to avoid getting rid of more CO2.

3) P_CO2 increases.

Front 51

Final correction of metabolic alkalosis involves what?

Back 51

Excretion of excess HCO3- in urine.

Front 52

How does volume contraction prevent Excretion of excess HCO3- in urine in metabolic alkalosis?

Back 52

RAA is activated and stimulate HCO3- reabsorption.

Front 53

Results from primary decrease in respiratory rate

Back 53

Respiratory acidosis.

CO2 isn't getting blown off.

Front 54

Where does buffering occur in respiratory acidosis?

Back 54

Intracellularly.

Renal compensation includes increased excretion of H+ as titratable acid and NH and increased reabsorption of both filtered and New HCO3-.

Front 55

results from primary increase in respiratory rate causing loss of CO2

Back 55

Respiratory alkalosis

Front 56

What is renal compensation of respiratory alkalosis?

Back 56

Decreased reabsorption of filtered and "new" HCO3-

Front 57

Normal values of
A) HCO3-
B) P_CO2
C) pH

Back 57

A) 24 mEq/L
B) 40 mm Hg
C) 7.35-7.45

Front 58

primary hyperaldosteronism (conn syndrome) causes what?

Back 58

Metabolic alkalosis.

Increase H+ secretion and new bicarb reabsorption.