VI: Acid-Base Physiology Flashcards
Acidemia range
pH<7.35
Alkalemia range
pH>7.45
Intracellular and extracellular pH
Intracellular pH (7.2) < Extracellular pH Intracellular pH is more acidic
Arterial pH is slightly
Alkaline, pH=7.4
Volatile acid definition
CO2, produced during digestion (end product of metabolism)
Nonvolatile acid definition
Produced from incomplete metabolism
EX. lactic acid
Excretion of volatile acids by
Lungs
CO2
Excretion of nonvolatile acids by
Kidney
Volatile acid into bicarbonate
CO2 + H2O H2CO3 HCO3- + H+
Enzyme involved in the reaction of CO2 into bicarbonate
Carbonic anhydrase
Under pathophysiologic states, B-hydroxybutyric acid and acetoacetic acid formed from
Untreated diabetes mellitus
Under pathophysiologic states, lactic acid formed from
Exercise and hypoxic tissue
Under pathophysiologic states, salicylic acid formed from
Aspirin overdose
Under pathophysiologic states, formic acid formed from
Methanol ingestion
Which acid must be buffered before being excreted by kidneys
Nonvolatile acids
Which compensation takes longer, renal or respiratory
Renal, respiratory compensation is very fast
Major buffers of EXTRACELLUAR fluid are
Bicarbonate and phosphate
Used to maintain the pH stable before they are excreted in urine
Bicarbonate buffering
H2O + CO2 H2CO3 HCO3- + H+
Phosphate buffering
H2PO4 < –> HPO4^2- + H+
Major buffers of INTRACELLULAR fluid are
Organic phosphates and proteins
Hb most significant
Henderson-Hasselbacch equation used to
Calculate pH of arterial blood pressure
pH = pK + log [A-]/[HA]
pH = 6.1 + log[HCO3-]/(0.3 x pCO2)
In reabsorption of filtered HCO3-, how much of it is reabsorbed
99.9%
Why is HCO3- rebasorbed
To ensure that the major EXTRACELLULAR BUFFER is conserved
Reabsorption of HCO3- in Proximal Tubule
80%
Reabsorption of HCO3- in Thick Ascending Limb in loop of Henle
10%
Reabsorption of HCO3- in A-Intercalated Cells of distal nephron
9.9%
Calculation of reabsorption
Glomerular filtration rate x Plasma [HCO3-] x Excretion rate of HCO3-
Reabsorption rate of HCO3- with numbers:
180L/d x 24mEq/L x 2mEq/d = 4318mEq/d
Meaning of reabsorption
Fluids going back to the vessels
Meaning of secretion
Fluids going into the renal tube
In the reabsorption of HCO3-, there is also reabsorption of
Na+
Is there NET SECRETION of H+
NO
NBC1:
Electronic Na+/HCO3- cotransporter 1
AE1:
Anion exchanger 1 (Cl-)
NHE-3:
Na+/H+ antitransporter 3
EFFECT OF FILTERED LOAD When does HCO3- absorption mechanism become saturated
When [plasma] > 40mEq/L –> metabolic alkalosis
When reabsorption mechanism saturated due to metabolic alkalosis,
Non-reabsorbed HCO3- is excreted in urine so that [blood] decreases to normal
EFFECT EXTRACELLULAR VOLUME, a decrease in ECV will activate the
Renin-angiotensin II-aldosterone
What stimulated the renin-angiotensin II-aldosterone
Na+/H+ exchange (NHE-3), stimulated HCO3- reabsorption
An increase in HCO3- reabsorption will cause
Contraction alkalosis from an increased pH in blood (more alkaline)
EFFECT OF PCO2
Increased pCO2 = Increased HCO3- reabsorption (bc CO2 is considered an acid, we want to lower the pH)
Decreased pCO2 = Decreased HCO3- reabsorption (we want to increase the pH)
Why dont we want direct elimination of H+ in urine
Bc it would make the urine pH=1.3
Which is the most important buffer due to increased concentration in urine
Phosphate
How much phosphate reabsorbed
85%
How much phosphate left to be excretes as titrable acid
15%
1st mechanism for H+ secretion is
H+ATPase stimulated by aldosterone
2nd mechanism for H+ secretion
H+/K+ATPase
Amount of H+ excreted depends on
Amount of acid buffer available
Blood vs urine pH
Blood = 7.4 Urine = 4.4
When does H+ excretion stop
When pH of urine reached 4.4
Other mechanism used asides from HPO4-
Excretion of H+ as NH4+ + HCO3-
Why is there another mechanism asides from phosphate
Because if not, excretion would be limited by the amount of phosphate in urine
Segments in nephron participating in H+ excretion as NH4+
Proximal tubule
Thick ascending limb
A-intercalated cells
Proximal tubule function in H+ excretion as NH4+
Proximal tubule, NH4+ secreted by Na+ - H+ exchange
Thick ascending limb function H+ excretion as NH4+
Thick ascending limb, NH4+ secretion by proximal tubule is REABSORBED
A-intercalated cells function in H+ excretion as NH4+
A-intercalated cells, NH3+ and H+ secreted into lumen
In proximal tubule, which Aa produces HCO3-
Glutamine
Glutamine in proximal tubule separates into
a-ketoglutarate
NH4+
In thick ascending limb, what happens with NH4+
It is reabsorbed, participates in counter-current multiplication
In a-intercalated cells, NH3
Can diffuse so it goes directly to lumen from blood
For each H+ secreted, how many HCO3-
One new HCO3- syntehtised and reabsorbed
Effect of urinary pH on excretion of NH4+
pH decreases = increase in NH4 buffer = less NH3
A decreased NH3 will cause a greater gradient for NH3 diffusion from interstitium to lumen
Effect of acidosis on NH3 synthesis
NH3 synthesis depends on how much H+ to be excreted
In chronic acidosis, there is an
Increased NH3+ synthesis of proximal tubule
Why does hyperkalemia inhibit NH3 synthesis
K+ will move into cell, causing H+ out of cell
Causing an increase in intracellular pH (more alkaline)