Acid-Base Physiology Flashcards
(17 cards)
1
Q
What is the normal pH range? What range is compatible with/necessary for life?
A
- normal ph: 7.4 (7.37-7.42)
- values outside the range of 6.8-8.0 are incompatible with life
2
Q
What are the three general mechanisms the body uses to maintain a normal pH? Which happen quickly?
A
- buffers: occurs rapidly
- respiratory mechanisms (excrete CO2): occurs rapidly
- renal mechanisms (reabsorb HCO3-, secrete H+): occurs slowly
3
Q
What is volatile acid? What about fixed acid? What processes produce each? How is each excreted?
A
- volatile acid is CO2; it is produced by aerobic metabolism
- fixed (or non-volatile acid) is produced by the catabolism of proteins and phospholipids; sulfuric acid, phosphoric acid, ketoacids, lactic acid
- CO2 is excreted by respiration, fixed acids are excreted by renal filtration
- this means that CO2 only needs to be buffered for a little while (because it is quickly excreted), while fixed acids need to be buffered for a longer period before they are excreted
4
Q
What are the major ECF buffers? Which is the most important and why? What are the major ICF buffers? Which is the most important?
A
- ECF: bicarbonate and inorganic phosphate
- bicarbonate is more important because of its conversion into CO2; this makes it readily excretable!
- ICF: proteins (such as Hb and albumin*) and organic phosphate
- most important is Hb (especially deoxyhemoglobin)
- *albumin can bind either H+ or Ca2+, which explains the development of hypercalcemia with acidosis and hypocalcemia with alkalosis
5
Q
How is fixed H+ excreted?
A
- fixed H+ is non-volatile and therefore must be excreted by the kidneys
- it is excreted either as titratable acid (this is when it is buffered by urinary inorganic phosphate to form H2PO4-) or as ammonium (buffered by ammonia to form NH4+)
- note that both processes of converting H+ into titratable acid or into NH4+ generate new HCO3- (this new HCO3- is used to replace the HCO3- currently being used to buffer the fixed H+ in the blood)
- (normally, 40% is as titratable acid, 60% as ammonium)
6
Q
How much HCO3- is normally reabsorbed by the kidneys? Where does the reabsorption take place? How is bicarbonate reabsorbed?
A
- virtually 100% of bicarb is reabsorbed (unless the concentration is too high, as in alkalosis)
- majority of reabsorption occurs in the proximal tubule (essentially, it gets reabsorbed with Na+)
- these cells have luminal Na+-H+ exchangers (brings Na+ into the cell and pumps H+ out); the H+ in the lumen combines with the HCO3- to form H2CO3
- H2CO3 is acted on by carbonic anhydrase in the brush border to form CO2 and H2O; both easily enter the cell
- intracellular carbonic anhydrase then reverses the reaction to regenerate H+ and HCO3-; the H+ is pumped back out into the lumen and the HCO3- is reabsorbed into the blood
- *(the H+ is essentially constantly recycled; therefore, there is no net increase of H+, so the luminal pH does not drop)
7
Q
What is contraction alkalosis? What can cause it?
A
- contraction alkalosis is the development of an alkalosis in response to a drop in ECF volume (volume contraction)
- the drop in ECF triggers RAAS, which promotes Na+ reabsorption to raise volume levels
- since HCO3- is reabsorbed with Na+, an alkalosis can develop as a result
- can be caused by loop diuretics, thiazide diuretics, vomiting
8
Q
How and where is fixed acid excreted by the kidneys as titratable acid?
A
- (titratable acid is H+ buffered with urinary inorganic phosphate; normally 40% of fixed acid is excreted in this form)
- H+ is secreted by the alpha-intercalated cells of the distal tubule and the collecting duct (these cells have CA that generates the H+)*
- 2 mechanisms of secretion: via the H+-ATPase pump and via the H+-K+-ATPase pump (pumps K+ into cell for reabsorption)
- once in the lumen, the H+ is buffered by inorganic phosphate (HPO42-) to form titratable acid (H2PO4-), which is excreted
- *this means that this process generates NEW bicarbonate
9
Q
How and where is fixed acid excreted by the kidneys as ammonium?
A
- (ammonium is H+ buffered with ammonia, NH3; normally 60% of fixed acid is excreted in this form)
- H+ is secreted by the proximal tubule, thick ascending dumb, and alpha-intercalated cells of the collecting duct (these cells have CA that generates the H+)*
- proximal tubule cells have a luminal Na+-H+ exchanger (Na+ reabsorption, H+ secretion)
- alpha-intercalated cells have luminal H+-ATPase pumps and H+-K+-ATPase pumps
- once in the lumen, H+ is bound to ammonia (NH3) to form ammonium (NH4+); the ammonia is a metabolic product of filtered glutamine
- *this means that this process generates NEW bicarbonate
10
Q
What role does potassium have in the excretion of fixed acid as ammonium? What can develop from hyperkalemia as a result?
A
- potassium can inhibit ammonia (NH3) synthesis
- hyperkalemia will result in renal tubular acidosis as the secreted H+ will be free instead of bound and buffered by ammonia
11
Q
Which ions are measured? What is the anion gap? What is the normal value?
A
- measured cations: Na+
- measured anions: HCO3- and Cl-
- electroneutrality exists, BUT the concentration of measured cations (Na+) is greater than that of the measured anions (HCO3- and Cl-)
- therefore, there must be some unmeasured anions (these are largely organic anions) contributing to the electroneutrality: this is the “anion gap”
- normal value for anion gap (the amount of unmeasured anions) is 8-16 mEq/L
12
Q
What does the anion gap value help us differentiate between? Explain.
A
- the anion gap is used to help diagnose the differentials of metabolic acidosis
- in metabolic acidosis, the concentration of HCO3- is lowered; in order for electroneutrality to be maintained, either Cl- or the unmeasured anions must be increased
- if anion gap is normal: diarrhea, renal tubular acidosis for example; this means that Cl- is increased instead
- if anion gap is increased: DKA, starvation, lactic acidosis, chronic renal failure, poisons; these conditions result in the accumulation of organic anions (unmeasured anions) as these are the conjugate bases of the organic acids developed in these disorders
13
Q
What is the arterial blood profile of metabolic acidosis? What can cause a metabolic acidosis? How soon does the renal correction take place? Does hyperkalemia always develop?
A
- metabolic acidosis: low pH, low HCO3-, low PaCO2 (because of immediate respiratory compensation as hyperventilation)
- the drop in HCO3- is due to an increase in fixed acid or due to loss of HCO3- (via diarrhea or renal tubular acidosis)
- renal correction (excess H+ is excreted and new HCO3- is made) occurs several days later
- as H+ accumulates, it enters cells in exchange for K+ (maintains electroneutrality), so hyperkalemia can develop; HOWEVER, it does NOT develop in cases where there is an accumulation of organic acids because H+ enters cells with the organic anion (the conjugate base of the organic acid) here, so there is no need for the K+ exchange, so no hyperkalemia will develop
14
Q
What is the arterial blood profile of respiratory acidosis? What can cause a respiratory acidosis? What form of compensation will take place?
A
- respiratory acidosis: low pH*, high PaCO2, high HCO3- (renal compensation after a few hours)
- caused by hypoventilation (via a depressed medullary respiratory center with opiates or O2 therapy), respiratory paralysis, airway obstruction, failure of CO2 to diffuse
- renal compensation results in an increase in H+ excretion and an increase in HCO3- reabsorption/synthesis
- *note that chronic cases of respiratory acidosis with have a relatively normal pH because of the long-term renal compensation
15
Q
What is the arterial blood profile of metabolic alkalosis? What can cause a metabolic alkalosis? What complicates the necessary renal correction? Does hypokalemia always develop?
A
- metabolic alkalosis: high pH, high HCO3-, high PaCO2 (because of immediate hypoventilation)
- increase in HCO3- is driving factor, caused by a loss of fixed acid (via vomiting, hyperaldosteronism), contraction alkalosis (diuretics)
- hypokalemia commonly develops as the intracellular buffers are releasing H+, which is pumped out of the cell in exchange for K+ (furthermore, in volume contraction, the resulting activation of RAAs increases K+ excretion, further contributing to the hypokalemia)
- renal correction involves secretion of the excess HCO3-; however this is often complicated by ECF contraction (commonly accompanies metabolic alkalosis): volume contraction triggers RAAS, AgII increases proximal tubule reabsorption of HCO3- (not what we want) and aldosterone increases reabsorption/synthesis of HCO3- by the alpha-intercalated cells (not what we want)
16
Q
What is the arterial blood profile of respiratory alkalosis? What can cause a respiratory alkalosis? What form of compensation will take place?
A
- respiratory alkalosis: high pH*, low PaCO2, low HCO3- (renal compensation after a few hours)
- caused by hyperventilation (hysteria, sepsis, neuro disorder), hypoxemia, mechanical ventilation
- renal compensation results in a decrease in H+ excretion and a decrease in HCO3- reabsorption/synthesis
- *in chronic cases, the pH is largely normal due to long-term renal compensation
17
Q
What is type 1 renal tubular acidosis? Type 2? Type 4? What does each result in?
A
(RTA is characterized by poor urinary acidification, leading to acidemia)
- type 1 RTA: (AKA distal/classic RTA) alpha-intercalated cells fail to secrete H+ and reabsorb K+; leads to severe acidemia and hypokalemia
- type 2 RTA: (AKA proximal RTA) proximal tubule fails to reabsorb HCO3-; leads to a moderate acidemia and hypokalemia
- type 4 RTA: due to HYPOaldosteronism; leads to a mild acidemia and HYPERkalemia
