APMLE Part 1 Renal and Acid-Base Physiology Questions
With Complete Solutions
What produces CO2 and what happens to it when it is produced?
Produced during the aerobic metabolism of cells and combines
with H20 to form weak acids H2CO3 which dissociated into H+
and HCO3- during reactions
uses CARBONIC ANHYDRASE
What the non-volatile acids?
Sulfuric Acid (from protein) and Phosphoric Acid (a product of
phospholipid catabolism)
Also: ketoacids, lactic acid, and salicyclic acid
What is the major extracellular buffer?
HCO3- which is made from CO2 and H2O
the pK is 6.1
What is a minor extracellular buffer?
Phosphate H2PO4 and its buffer pair is 6.8
What are the major intracellular buffers?
Organic Phosphates (AMP, ADP, ATP, 2,3 DPG)
Proteins (imidazole, and alpha amino groups on proteins that
have PKs). Hemoglobin
,What is the Henderson Hasselbach equation?
pH = pK + log (Base/Acid)
How is HCO3- absorbed?
1) H+ and HCO3- are produced in the proximal tubule cells
from CO2 and H2O. CO2 and H2O combine to form H2CO3,
catalyzed by INTRACELLULAR CARBONIC ANHYDRASE;
H2OCO3 dissociates into H+ and HCO3-. H+ is secreted into
the lumen via the Na+ H+ exchange in the luminal membrane
2) In the lumen secreted H+ combines with filtered HCO3- to
form H2CO3, which dissociated into CO2 and H2O catalyzed
by BRUSH BORDER CARBONIC ANHYDRASE
3) The process results in net reabsorption filtered HCO3-,
however it does not result in net secretion of H+
When will HCO3- be secreted in the urine?
when the filleted load exceeds the reabsorptive capacity and
HCO3- increases during metabolic alkalosis
What happens in the kidneys if PCO2 is increased?
results in increased rates of HCO3- reabsorption because the
supply of intracellular H+ for secretion is increased. This
mechanism is the basis for the renal compensation for
respiratory acidosis.
What happens in the kidneys if PCO2 is decreased?
,result in decreased rates of HCO3- reabsorption because the
supply of intracellular H+ for secretion is decreased. This
mechanism is the basis for the renal compensation for
respiratory alkalosis.
What happens to HCO3- reabsorption in an ECF volume
expansion?
results in decreased HCO3- reabsorption
What happens to HCO3- reabsorption in an ECF volume
contraction?
results in increased HCO3- reabsorption
What is angiotensin II's effect on HCO3-?
stimulates Na+-H+ exchange and thus increases HCO3−
reabsorption, con- tributing to the contraction alkalosis that
occurs secondary to ECF volume contraction.
What are the two mechanisms that H+ is excreted by?
1) Excretion of H+ as titratable H2PO4-
2) Excretion of H+ as NH4+
What is the mechanism of H+ excretion as titratable H2PO4-?
(1) H+ and HCO3- are produced in the cell from CO2 and H2O.
The H+ is secreted into the lumen by an H+-ATPase, and the
HCO3- is reabsorbed into the blood ("new" HCO3-). In the
urine, the secreted H+ combines with filtered HPO4-2 to form
H2PO4-, which is excreted as titratable acid. The H+-ATPase is
increased by aldosterone.
, (2) This process results in net secretion of H+ and net
reabsorption of newly synthesized HCO3-. +
(3) As a result of H secretion, the pH of urine becomes
progressively lower. The minimum urinary pH is 4.4.
(4) The amount of H+ excreted as titratable acid is determined
by the amount of urinary buffer and the pK of the buffer.
What amino acid produces NH3?
NH3 is produced in renal cells from glutamine. It diffuses down
its concentration gradient from the cells into the lumen.
How NH4+ formed in the renal cells?
H+ and HCO3- are produced in the cells from CO2 and H2O.
The H+ is secreted into the lumen via an H+-ATPase and
combines with NH3 to form NH4+, which is excreted (diffusion
trapping). The HCO3− is reabsorbed into the blood ("new"
HCO3−).
The lower pH in the tubular fluid what happens to the excretion
rate of H+ as NH4+?
The lower the pH of the tubular fluid, the greater the excretion
of H+ as NH4+; at low urine pH, there is more NH4+ relative to
NH3 in the urine, thus increasing the gradient for NH3 diffusion.
In acidosis, an adaptive increase in NH3 synthesis occurs and
aids in the excretion of excess H+.
With Complete Solutions
What produces CO2 and what happens to it when it is produced?
Produced during the aerobic metabolism of cells and combines
with H20 to form weak acids H2CO3 which dissociated into H+
and HCO3- during reactions
uses CARBONIC ANHYDRASE
What the non-volatile acids?
Sulfuric Acid (from protein) and Phosphoric Acid (a product of
phospholipid catabolism)
Also: ketoacids, lactic acid, and salicyclic acid
What is the major extracellular buffer?
HCO3- which is made from CO2 and H2O
the pK is 6.1
What is a minor extracellular buffer?
Phosphate H2PO4 and its buffer pair is 6.8
What are the major intracellular buffers?
Organic Phosphates (AMP, ADP, ATP, 2,3 DPG)
Proteins (imidazole, and alpha amino groups on proteins that
have PKs). Hemoglobin
,What is the Henderson Hasselbach equation?
pH = pK + log (Base/Acid)
How is HCO3- absorbed?
1) H+ and HCO3- are produced in the proximal tubule cells
from CO2 and H2O. CO2 and H2O combine to form H2CO3,
catalyzed by INTRACELLULAR CARBONIC ANHYDRASE;
H2OCO3 dissociates into H+ and HCO3-. H+ is secreted into
the lumen via the Na+ H+ exchange in the luminal membrane
2) In the lumen secreted H+ combines with filtered HCO3- to
form H2CO3, which dissociated into CO2 and H2O catalyzed
by BRUSH BORDER CARBONIC ANHYDRASE
3) The process results in net reabsorption filtered HCO3-,
however it does not result in net secretion of H+
When will HCO3- be secreted in the urine?
when the filleted load exceeds the reabsorptive capacity and
HCO3- increases during metabolic alkalosis
What happens in the kidneys if PCO2 is increased?
results in increased rates of HCO3- reabsorption because the
supply of intracellular H+ for secretion is increased. This
mechanism is the basis for the renal compensation for
respiratory acidosis.
What happens in the kidneys if PCO2 is decreased?
,result in decreased rates of HCO3- reabsorption because the
supply of intracellular H+ for secretion is decreased. This
mechanism is the basis for the renal compensation for
respiratory alkalosis.
What happens to HCO3- reabsorption in an ECF volume
expansion?
results in decreased HCO3- reabsorption
What happens to HCO3- reabsorption in an ECF volume
contraction?
results in increased HCO3- reabsorption
What is angiotensin II's effect on HCO3-?
stimulates Na+-H+ exchange and thus increases HCO3−
reabsorption, con- tributing to the contraction alkalosis that
occurs secondary to ECF volume contraction.
What are the two mechanisms that H+ is excreted by?
1) Excretion of H+ as titratable H2PO4-
2) Excretion of H+ as NH4+
What is the mechanism of H+ excretion as titratable H2PO4-?
(1) H+ and HCO3- are produced in the cell from CO2 and H2O.
The H+ is secreted into the lumen by an H+-ATPase, and the
HCO3- is reabsorbed into the blood ("new" HCO3-). In the
urine, the secreted H+ combines with filtered HPO4-2 to form
H2PO4-, which is excreted as titratable acid. The H+-ATPase is
increased by aldosterone.
, (2) This process results in net secretion of H+ and net
reabsorption of newly synthesized HCO3-. +
(3) As a result of H secretion, the pH of urine becomes
progressively lower. The minimum urinary pH is 4.4.
(4) The amount of H+ excreted as titratable acid is determined
by the amount of urinary buffer and the pK of the buffer.
What amino acid produces NH3?
NH3 is produced in renal cells from glutamine. It diffuses down
its concentration gradient from the cells into the lumen.
How NH4+ formed in the renal cells?
H+ and HCO3- are produced in the cells from CO2 and H2O.
The H+ is secreted into the lumen via an H+-ATPase and
combines with NH3 to form NH4+, which is excreted (diffusion
trapping). The HCO3− is reabsorbed into the blood ("new"
HCO3−).
The lower pH in the tubular fluid what happens to the excretion
rate of H+ as NH4+?
The lower the pH of the tubular fluid, the greater the excretion
of H+ as NH4+; at low urine pH, there is more NH4+ relative to
NH3 in the urine, thus increasing the gradient for NH3 diffusion.
In acidosis, an adaptive increase in NH3 synthesis occurs and
aids in the excretion of excess H+.
