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*$)$($&(*$@IHRJOIoewyYEUIUEUEq
BOD: RENAL PATHOPHYSIOLOGY ACID BASE…
This document covers renal pathophysiology with a focus on acid-base
disorders and their relationship to fluid and electrolyte balance. It includes
key concepts such as metabolic and respiratory acid-base disturbances,
renal regulation of pH, electrolyte shifts, and compensatory mechanisms.
The material is designed to support nursing and health science exam
preparation by strengthening understanding of renal system function and
clinical acid-base balance.
2Queries /ANSWERS
0
2
6
1 What is normal blood pH? 7.38 to 7.42
2 What is the [H+] at a physiologic 40 nEq/L
pH of 7.40?
3 normal arterial PCO2? 36-44 mmHg
4 What is the equation for the (lungs) CO2 + H2O H2CO3 H+ + HCO3- (kidneys).
carbonic acid buffer system?
5 What is a normal plasma [HCO3-]? about 25 mEq/L
6 Where does most bicarbonate PCT. The distal nephron has almost no ability to
reabsorption happen? reab HCO3-
7 Explain the process of 1\. There is an Na+/K+ ATPase on the
reabsorption of bicarb at the PCT. anti-lumenal side of the proximal tubule cell. This
Include ions, transporters, etc. lowers the [Na+] in the cell. 2\. Driven by the
gradient above, an Na+/H+ antiporter brings Na+
into the cell and secretes H+ into the tubule
lumen. 3\. The H+ sec into the lumen combines
with bicarb to make H2CO3, which then forms
H2O and CO2 with the help of carbonic
anhydrase. 4\. H2O and CO2 diffuse into the cell,
reform H2CO3 --> HCO3- and H+. 5\. The H+ is
secreted back into the lumen to combine with
another molecule of bicarb. 6\. The HCO3- in the
cell moves into the peritubular fluid via a
Na+/HCO3- symporter. This symporter is driven
by an ELECTRICAL GRADIENT created by the
ATPase and the overall negative charge within
the cell.
8 True or false: the kidney will adjust False. Bicarb reabsorption is saturated at 25
to bicarb levels above 25 mEq/L by mEq/L. Consequently, the admin of even a large
increasing reabsorption along the amt of bicarb cannot result in a sustained serum
nephron. increase.
, BOD: RENAL PATHOPHYSIOLOGY ACID BASE DISORDERS STUDY GUIDE KIDNEY…
2Queries /ANSWERS
0
2
6
9 Where along the nephron does Mostly in the collecting tubules, by H+ ATPases
acid get secreted? How? (facilitated by aldosterone)
10 What effect does aldosterone have 1\. Aldosterone enters principal cell, opening
on the cells of the cortical lumenal Na+ channels, and inc Na+/K+ ATPase
collecting tubule? activity. 2\. Na+ moves from the lumen into the
principal cells, "leaving behind" a negative
charge. 3\. This gradient causes K+ to move out
of the principal cells into the lumen and H+ to
move out of the alpha-intercalated cells into the
lumen. 5\. Aldosterone also directly stims the H+
ATPase in the alpha-intercalated cell, increasing
acid sec. An HCO3- is generated in this process.
The bicarb moves into the peritubular fluid via a
Cl-/HCO3- antiporter. At a sep location on the
antilumenal side, a Cl- moves through a channel
into the peritubular fluid to maintain electric
neutrality.
11 What is the most important buffer Ammonia (NH3).
in the urine?
12 What would be the consequences Reduced renal acid excretion and a fall in blood
of failing to make enough urinary pH.
ammonia?
13 Where is urinary ammonia In the cells of the PCT.
synthesized?
14 What molecule is ammonia Ammonia is synthesized from glutamine.
synthesized from? What is the Alpha-ketoglutarate is also formed (and then
other biproduct besides becomes HCO3- and moves into peritubular fluid)
ammonia?
15 What is the path that urinary 1\. Sec out of the PCT cells by acting like H+ and
ammonia/um takes? hijacking the H+/Na+ antiporter (it becomes a
NH4+/Na+ antiporter). 2\. Travels to the thick
ascending limb and is transported into the
medullary interstitum by mimicing K+ on the
Na+/K+/2Cl- transporter. 3\. Ammonium
dissociates to ammonia in the interstitum. 4\.
Ammonia diffuses down conc grad into the
collecting duct. 5\. Ammonia combines with H+ to
become ammonium. 6\. Eventually exc as NH4Cl
to maintain electrical neutrality.
*$)$($&(*$@IHRJOIoewyYEUIUEUEq
BOD: RENAL PATHOPHYSIOLOGY ACID BASE…
This document covers renal pathophysiology with a focus on acid-base
disorders and their relationship to fluid and electrolyte balance. It includes
key concepts such as metabolic and respiratory acid-base disturbances,
renal regulation of pH, electrolyte shifts, and compensatory mechanisms.
The material is designed to support nursing and health science exam
preparation by strengthening understanding of renal system function and
clinical acid-base balance.
2Queries /ANSWERS
0
2
6
1 What is normal blood pH? 7.38 to 7.42
2 What is the [H+] at a physiologic 40 nEq/L
pH of 7.40?
3 normal arterial PCO2? 36-44 mmHg
4 What is the equation for the (lungs) CO2 + H2O H2CO3 H+ + HCO3- (kidneys).
carbonic acid buffer system?
5 What is a normal plasma [HCO3-]? about 25 mEq/L
6 Where does most bicarbonate PCT. The distal nephron has almost no ability to
reabsorption happen? reab HCO3-
7 Explain the process of 1\. There is an Na+/K+ ATPase on the
reabsorption of bicarb at the PCT. anti-lumenal side of the proximal tubule cell. This
Include ions, transporters, etc. lowers the [Na+] in the cell. 2\. Driven by the
gradient above, an Na+/H+ antiporter brings Na+
into the cell and secretes H+ into the tubule
lumen. 3\. The H+ sec into the lumen combines
with bicarb to make H2CO3, which then forms
H2O and CO2 with the help of carbonic
anhydrase. 4\. H2O and CO2 diffuse into the cell,
reform H2CO3 --> HCO3- and H+. 5\. The H+ is
secreted back into the lumen to combine with
another molecule of bicarb. 6\. The HCO3- in the
cell moves into the peritubular fluid via a
Na+/HCO3- symporter. This symporter is driven
by an ELECTRICAL GRADIENT created by the
ATPase and the overall negative charge within
the cell.
8 True or false: the kidney will adjust False. Bicarb reabsorption is saturated at 25
to bicarb levels above 25 mEq/L by mEq/L. Consequently, the admin of even a large
increasing reabsorption along the amt of bicarb cannot result in a sustained serum
nephron. increase.
, BOD: RENAL PATHOPHYSIOLOGY ACID BASE DISORDERS STUDY GUIDE KIDNEY…
2Queries /ANSWERS
0
2
6
9 Where along the nephron does Mostly in the collecting tubules, by H+ ATPases
acid get secreted? How? (facilitated by aldosterone)
10 What effect does aldosterone have 1\. Aldosterone enters principal cell, opening
on the cells of the cortical lumenal Na+ channels, and inc Na+/K+ ATPase
collecting tubule? activity. 2\. Na+ moves from the lumen into the
principal cells, "leaving behind" a negative
charge. 3\. This gradient causes K+ to move out
of the principal cells into the lumen and H+ to
move out of the alpha-intercalated cells into the
lumen. 5\. Aldosterone also directly stims the H+
ATPase in the alpha-intercalated cell, increasing
acid sec. An HCO3- is generated in this process.
The bicarb moves into the peritubular fluid via a
Cl-/HCO3- antiporter. At a sep location on the
antilumenal side, a Cl- moves through a channel
into the peritubular fluid to maintain electric
neutrality.
11 What is the most important buffer Ammonia (NH3).
in the urine?
12 What would be the consequences Reduced renal acid excretion and a fall in blood
of failing to make enough urinary pH.
ammonia?
13 Where is urinary ammonia In the cells of the PCT.
synthesized?
14 What molecule is ammonia Ammonia is synthesized from glutamine.
synthesized from? What is the Alpha-ketoglutarate is also formed (and then
other biproduct besides becomes HCO3- and moves into peritubular fluid)
ammonia?
15 What is the path that urinary 1\. Sec out of the PCT cells by acting like H+ and
ammonia/um takes? hijacking the H+/Na+ antiporter (it becomes a
NH4+/Na+ antiporter). 2\. Travels to the thick
ascending limb and is transported into the
medullary interstitum by mimicing K+ on the
Na+/K+/2Cl- transporter. 3\. Ammonium
dissociates to ammonia in the interstitum. 4\.
Ammonia diffuses down conc grad into the
collecting duct. 5\. Ammonia combines with H+ to
become ammonium. 6\. Eventually exc as NH4Cl
to maintain electrical neutrality.
