Page 96 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Development of Alkalosis
–
The pH of blood depends on the ratio of HCO 3 (→ A5). Thus, the kidneys ability to eliminate
–
to CO 2 concentration: HCO 3 is compromised and the result is vol-
HCO ume depletion alkalosis. Hyperaldosteronism
pH = pK + log 3 can lead to alkalosis without volume deple-
CO 2
tion.
! Parathyroid hormone (PTH) normally inhib-
pK contains the dissociation constant of H 2 CO 3
–
and the reaction constant of CO 2 to H 2 CO 3 . Al- its HCO 3 absorption in the proximal tubules.
kalosis (pH > 7.44) thus occurs either when Hypoparathyroidism can thus lead to alkalosis.
Acid–Base Balance pocapnia, respiratory alkalosis), or that of from the NH 4 generated by amino acid ca- –
the CO 2 concentration in blood is too low (hy-
! The liver forms either glutamine or urea
+
–
HCO 3 is too high (metabolic alkalosis).
tabolism. The formation of urea requires, in
+
Respiratory alkalosis occurs in hyperventi-
addition to two NH 4 , the input of two HCO 3
that are lost when urea is excreted. (However,
lation (→ A3 and p. 82). Causes include emo-
+
NH 4 is split off from glutamine in the kidney
tional excitement, salicylate poisoning, or
damage to the respiratory neurons (e.g., by in-
and then excreted as such). In liver failure he-
Respiration, flammation, injury, or liver failure). Occasion- patic production of urea is decreased (→ A7),
–
the liver uses up less HCO 3 , and alkalosis de-
ally a lack of O 2 supply in the inspiratory air
velops. However, in liver failure respiratory al-
(e.g., at high altitude) causes increased ventila-
kalosis often predominates as a result of dam-
tion resulting in an increased amount of CO 2
! An increased supply of alkaline salts or mo-
Numerous disorders can lead to metabolic
4 being expired. age to the respiratory neurons (see above).
(i.e., non-respiratory) alkalosis: bilization of alkaline salts from bone (→ A2),
! In hypokalemia the chemical gradient for K + for example, during immobilization, can cause
across all cell membranes is increased. In some alkalosis.
cells this leads to hyperpolarization, which ! Metabolic activity may cause the accumu-
–
drives more negatively charged HCO 3 from lation of organic acids, such as lactic acid and
the cell. Hyperpolarization, for example, raises fatty acids. These acids are practically
–
HCO 3 efflux from the proximal (renal) tubule completely dissociated at blood pH, i.e., one
+
+
–
cell via Na (HCO 3 ) 3 cotransport (→ A4). The H is produced per acid. If these acids are me-
+
resulting intracellular acidosis stimulates the tabolized, H disappears again (→ A1). Con-
+
+
luminal Na /H exchange and thus promotes sumption of the acids can thus cause alkalosis.
–
+
H secretion as well as HCO 3 production in ! The breakdown of cysteine and methionine
+
the proximal tubule cell. Ultimately both pro- usually produces SO 4 2– + 2 H , the breakdown
+
cesses lead to (extracellular) alkalosis. of arginine and lysine produces H . Reduced
! In vomiting of stomach contents the body protein breakdown (e.g., as a result of a pro-
+
loses H (→ A6). What is left behind is the tein-deficient diet; → A8), reduces the
–
+
HCO 3 produced when HCl is secreted in the metabolic formation of H and thus favors the
–
parietal cells. Normally the HCO 3 formed in development of an alkalosis.
the stomach is reused in the duodenum to The extent to which the blood’s pH is
neutralize the acidic stomach contents and changed depends, among other factors, on the
only transiently leads to (weak) alkalosis. buffering capacity of blood, which is reduced
! Vomiting also reduces the blood volume. when the plasma protein concentration is low-
Edemas as well as extrarenal and renal loss of ered.
fluid can similarly result in volume depletion
(→ A4; see also p.122). Reduced blood volume
+
+
stimulates Na /H exchange in the proximal
–
tubules and forces increased HCO 3 reabsorp-
tion by the kidneys even in alkalosis. In addi-
86 tion, aldosterone is released in hypovolemia,
+
stimulating H secretion in the distal nephron
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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