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Renal Course > Renal Handling Of H+/HCO3- > Flashcards

Renal Handling Of H+/HCO3- Flashcards

1
Q

What is normal physiological pH?

A

7.35-7.45

Acidemia = < 7.35

Alkalosis = > 7.45

PH range that is comparable with life = 6.8-8.0
- anything outside of this range for an extended period of time = death

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2
Q

How does the concentration of protons change with respect to shortcut pH values?

A

Changes in 1.0 pH = 10x fold
- i.e: 7.0 ->6.0 pH =
1 x10^-7 -> 1 x 10^-6 H+ concentrations

Changes in 0.3 pH = 2x fold
- i.e 7.4 -> 7.1 pH = 4 x 10^-8 -> 8 x 10^-6

Changes in concentration fo H+ ions and pH exists on a logarithmic relationship, not linear

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3
Q

The three main mechanisms that contribute to maintaining pH in the normal range

A

1) buffering of H+ in both ECF/ICF
2) Respiratory compensation
3) Renal compensation

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4
Q

What are the most important extracellular buffers?

A

Bicarbonate: most important ECF buffer
HA form = CO2
A- form = HCO3-
- is the first line of defense when H+ is added or lost from the body
- normal HC03- concentration = 24 mEq/L
- CO2 form of bicarbonate is volatile and easily expired
- **when a strong acid is added to bicarbonate solutions = becomes carbonic acid and then dissociates into CO2/H20 and excreted via lungs

Phosphate
HA form = H2PO4(-)
A- form = HPO4(2-)
when a strong acid is added to HPO4(2-) it becomes H2PO4(-) which is excreted by the kidneys

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5
Q

Henderson-hasselbach equation purpose

A

CO2 from atmosphere combines with water to form carbonic acid spontaneously

Carbonic acid will break down into protons and bicarbonate via carbonic anhydrase into H+ and HCO3-

Net reaction: CO2 + H20 -> H+ + HCO3-

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6
Q

Henrys law

A

A concentration of a dissolved gas is directly related to its partial pressure

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7
Q

Why is bicarbonate buffer system more effective than phosphate buffer?

A

Bicarbonate (24 mmol/L) is much higher concentration that phosphate (1-2 mmol/L)

The acid form of bicarbonate is CO2 which is volatile and can be excreted via lungs

The base form of bicarbonate is HC03- which can be excreted via kidneys

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8
Q

How does calcium change in acidemia vs alkalemia?

A

Acidemia = ionized calcium (free)

  • albumin proteins release non ionized calcium to bind excess H+ ions
  • produces hypercalcemia

Alkalemia = non-ionized calcium (bound)

  • albumin proteins bind more calcium due to deficiency of H+ ions in blood
  • produces hypocalcemia
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9
Q

Most important intracellular buffers

A

Includes organic phosphates (ADP/ATP), DPG and proteins (especially hemoglobin which is most significant)

In order to be used, H+ has to get into cells via 1 of 3 ways:

  • 1) conditions where there is an excess or deficit of CO2 (respiratory acidosis)
  • 2) conditions where there is excess fixed acids in the blood (H+ can attach to lactate for example)
  • 3) conditions where there is excess H+ with no organic anion (switch’s with K+ to get into cell)
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10
Q

Reabsorption of filtered bicarbonate

A

1) bicarbonate binds to H+ ions that are secreted via sodium/H+ exchanger channels on the lumen surface of primarily the PCT (but also DCT and CD).
- forms carbonic acid via carbonic anhydrase

2) carbonic anhydrase cleaves carbonic acid into CO2/H20 which easily diffuse into the PCT cells

3) CO2/H20 then recombine into carbonic acid via carbonic anhydrase and then also break down into H+/HCO3- ions
- essentially step 1 in reverse

4) bicarbonate is then reabsorbed via Na+/bicarbonate cotransporter channels and Cl-/HCO3- exchangers on the basolateral surface

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11
Q

Where does excretion of titratable acid occur?

also one way to create new bicarbonate

A

In the a-intercalated cells of the collecting duct and very late DCT

1) secretes H+ ions into the lumen and bind to phosphate ions and generate H2PO4- which is excreted

2) a-intercalated cells use carbonic anhydrase to form and break apart carbonic acid into H+/HCO3- ions
- this bicarbonate is reabsorbed via bicarbonate/Cl- exchanges on the basolateral surface
- this is termed “new” bicarbonate

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12
Q

Excretion of NH4+ occurs where?

also the 2nd area to reabsorb new HCO3-

A

In PCT/TAL/(a)-intercalated cells
- (primarily PCT though)

1) ammonium ions (NH4+) are generated inside PCT cells via break down of glutamine -> glutamate +(NH4+)-> a-ketoglutarate -> HCO3-
- **this generates new HCO3- which is reabsorbed while also generating NH4+

2) these ammonium ions (NH4+) spontaneously break apart into NH3 + H+ so NH3 can leave the cell and go into the lumen
3) ammonia (NH3+) ions that are found in the lumen uptake H+ ions that get into the lumen via Na+/H+ exchanger channels found on lumen and form NH4+
4) NH4+ is readily excretable since it cant be reuptaken unless pathology is present

HCO3- made in step 1 is reabsorbed via Na+/HCO3- cotransporter on basolateral side

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13
Q

Winters formula

A

Gives the expected PCO2 based on a measured HCO3- concentration

Used to determine respiratory compensation for a metabolic acidosis

PCO2 = [(1.5 x HCO3-) + 8] +/-2

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14
Q

Anion gap

A

Anion gap = (Na+)-(Cl- + HCO3-)

  • normal = 8-12 mEq/L
  • high = > 12 mEq/L

Must check this if metabolic acidosis is present in a patient since this tells you possible underlying pathologies

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15
Q

How does intracellular and extracellular pH differ?

A

Intracellular =7.2

Extracellular = 7.4

Na+/H+ channels = move H+ out of ICF = more alkaline intracellular

Cl-/HCO3- channels = moves HCO3- out of cells = more acidic intracellular

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16
Q

Difference between Volatile and nonvolatile/fixed acids

A

Volatile acid = CO2

  • becomes carbonic acid (weaker acid) when combined with H20
  • dissociates into H+/HCO3- and travels through the blood to lungs. Here the reaction reverses and CO2 is expelled (or vise versa and regenerated)

Fixed acids = sulfuric, phosphoric acids, B-hydroxybutyric acid and AOA, lactic acid, formic acid, glycolic acid, oxalic acid (etc).
- cant be expelled by the lungs and instead needs to be buffered by body fluids until excreted by kidneys

17
Q

How do ATP and ADP work as buffers?

A

The phosphate groups on these molecules bind to H+ free ions

18
Q

how does hemoglobin work as a buffer?

A

As blood flows through capillaries, O2 is released and hemoglobin -> deoxyhemoglobin

Deoxyhemoglobin accepts CO2 which gets converted into carbonic acid and H+/HCO3-. HCO3- leaves the red blood cell but the H+ gets buffered by binding to the hemoglobin

primary reason behind why venous blood is only 0.03 lower in pH, despite having much larger amounts of CO2 than arterial blood

19
Q

What are the two ways that kidneys excrete fixed H+?

A

1) excretion of H+ bound to phosphate (H2PO4-)
2) excretion of H+ bound to NH3 (makes NH4+ which cant leave the renal lumen)

  • both methods generate new HCO3- which is reabsorbed in the a-intercalated cells*
  • this is to replenish the HCO3- that was used to buffer fixed acids
20
Q

How do you measure the reabsoption rate of HC03-?

A

Filtered load of HCO3- = (GFR) x ( plasma concentration)
- under normal conditions = (180L/day) x (24mEq/L)= 4320

Excretion rate of HCO3- is almost always 2 mEq/day (except in pathology)

reabsorption rate = (filtered load) - (excretion rate)
- under normal situations = 4318 mEq/day

the majority of this occurs in the PCT

21
Q

How does ECF expansion and contraction change bicarbonate reabsoption?

A

ECF volume expansion = inhibits HCO3- reabsorption

ECF volume contraction = promotes HCO3- reabsorption

this and the function of angiotensin-2 on increasing Na/H+ channel activity explains why contraction alkalosis occurs (volume contraction automatically leads to acute metabolic alkalosis)

22
Q

How does PCO2 levels affect HCO3- levels?

A

Directly proportional

1) in metabolic acidosis, there is more H+ present in the blood and filtrate, which leads to increased Na+/H+ activity in the PCT cells.
2) this increase in activity causes higher levels of H+ to be in the lumen which promotes more carbonic acid formation and subsequent HCO3- reabsoption

23
Q

Mechanism of excretion of titratable acid (H+ ions with urinary buffers (H2PO4- is msot common))

A

Excreted via a-intercalated cells of late DCT/CD
- use H+/ATPase channels (which are stimulated by aldosterone) and H+/K+/ATPase)

H+ that is secreted binds to free HPO3(2-) and forms titratable acid (H2PO4-) which is secreted

24
Q

what prevents over excretion of H+ ions?

A

The pH of urine
- once the pH of urine hits 4.4, no more H+ will be secreted (due to acidic gradient preventing H+ from being pushed in)

this is why it is important to have Phosphate, Bicarbonate and ammonium in the urine/filtrate since the presence fo these limits the speed at which the urine decreases form 7.4 -> 4.4

25
Q

What is the amount of fixed H+ production in the body from protein/phospholipid catabolism?

A

50 mEq/day

  • 20 mEq/day = excreted via phosphate acid/ titratable acid
  • 30 mEq/day = excreted via NH4+ ions
26
Q

How does acidosis and hyperkalemia affect NH3+ generation?

A

Hyperkalemia
- inhibits NH3 synthesis and reduces ability to excrete H+ as NH4+

Acidosis
- promotes NH3 synthesis and increases ability to excrete H+ as NH4+

27
Q

How does diabetic ketoacidosis and chronic renal failure change fixed H+ secretion?

A

Diabetic ketoacidosis

  • increases total fixed H+ to 500 mEq/L a day
  • causes increase glutamine metabolism and increased synthesis of NH3
  • increases NH3 and titratable acid levels

Chronic renal failure

  • normal levels of total fixed H+ (50mEq/L)
  • decreased levels of phosphate buffer (since GFR is lowered) and impaired NH3 synthesis in PCT cells
  • decreases levels of NH3 and titratable acid levels
28
Q

Causes of increased anion gap metabolic acidosis

A

MUDPILES

M = methanol 
U = uremia 
D = Diabetic ketoacidosis 
P = Propylene glycol 
I = Iron tablets 
L = lactic acidosis (ethanol OD) 
E = ethylene glycol 
S= Salicylate OD
29
Q

Causes of normal anion gap metabolic acidosis

A

“HARDASS”

H = hyperchloremia
A = addisons/adrenal insufficiency 
R = renal tubular acidosis 
D = diarrhea 
A = acetazolamide OD (Carbonic anhydrase Inhibtors) 
S = Sprionolactone (K+ sparring) 
S = Saline hyperinfusion
30
Q

How does vomiting cause metabolic alkalosis

A

Gastric parietal cells produce H+ and HCO3- from carbonic anhydrase. HCO3- is reabsorbed and H+ is secreted out with Cl- to form HCL

Under normal nonvomoting conditions, normal HCL concentrations reach the small intestine (with food) and stimulate the originally reabsorbed HCO3- to get excreted but he pancreas back into the small intestine to neutralize the HCL
- this does NOT occur in vomiting, which in turn leads to loss of H+ (from vomiting HCL) and increase of HCO3-

31
Q

How do loop and thiazides diuretics lead to metabolic alkalosis?

A

Volume contraction/ loss leads to increased angiotensin-2 and aldosterone which icnreases HCO3- absorption

32
Q

Renal tubular acidosis subtypes

A

all subtypes lead to hyperchloremic metabolic acidosis

Type 1 (distal)

  • caused by inability of a-intercalated cells to secrete H+ which leads to decreased HCO3- generation
  • leads to metabolic acidosis and hypokalemia
  • causes = autoimmune diseases, amphotericin B use, urinary tract obstruction

Type 2(proximal)

  • caused by PCT defects where HCO3- cannot be reabsorb properly
  • leads to metabolic acidosis and hypokalemia
  • causes = Fanconi syndrome, multiple myeloma, carbonic anhydrase Inhibtors

Type 4 (hyperkalemia)

  • caused by hypoaldosteronism or aldosterone resistance which leads to hyponatremia and hyperkalemia (since ENaC channels dont work) this prevents H+ and K+ secretion
  • leads to metabolic acidosis and hyperkalemia

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