Page 138 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Abnormalities of Calcium Balance
2+
Ca , as “intracellular transmitter”, mediates from bone and thus to hypercalcemia. Occa-
electromechanical coupling. It stimulates the sionally malignant tumors will, even in the ab-
release of neurotransmitters (synaptic trans- sence of skeletal metastases, produce bone-
mitters) and hormones, the secretory activity mobilizing hormones such as osteoclast-acti-
of exocrine glands and of a number of enzymes vating factor (OAF). Lastly, minerals in bone
(e.g., glycogenolysis, phospholipase A, adeny- will be mobilized on acute immobilization as-
lylcyclase, phosphodiesterases). Ca 2+ activates sociated with atrophy of inactivity. Increased
+
some K channels, for example, in the heart, enteric Ca 2+ absorption is brought about by an
Kidney, Salt and Water Balance meability of the basement membranes and pocalcemia is an increased excitability of mus-
+
2+
2+
excessive supply of Ca
where Ca -sensitive K channels take part in
and alkaline sub-
the process of repolarization. Extracellular
stances (milk-alkali syndrome).
2+
+
stabilizes Na channels, reduces the per-
The clinically most significant effect of hy-
Ca
cles and nerves with the occurrence of invol-
the tight junctions, and plays a role in blood
untary muscle spasms (tetany) and paresthe-
clotting.
2+ con-
The regulation of the extracellular Ca
sias (→ A4). The increased excitability is prob-
+
ably due to the lowered threshold of Na chan-
centration is, in the first instance, the task of
nels in hypocalcemia. In severe cases epileptic
PTH. It is normally released in hypocalcemia
2+
triggers a lengthening of the action potential
tion of Ca
(→ A1,A2). PTH stimulates the
in the heart because of the delayed activation
mobilization of calcium phosphate from bone,
+
of the K channels, resulting in prolongation
decreases the plasma concentration of phos-
5 and its action increases the plasma concentra- seizures may occur (→ p. 338). Hypocalcemia
phate by inhibiting its renal reabsorption, and of the ST segment and QT interval in the ECG.
stimulates the formation of calcitriol, which The effects of hypercalcemia (the condition
promotes the enteric absorption of Ca 2+ and is often asymptomatic) may include gastroin-
phosphate, and thus aids in the mineralization testinal symptoms (peptic ulcers due to stimu-
of the bones. lation of gastrin release and inhibition of pan-
–
Hypocalcemia (→ A1) can be the result of creatic HCO 3 -secretion by the Ca 2+ receptor,
reduced PTH release (hypoparathyroidism) or nausea, vomiting, constipation), polyuria (in-
effect (pseudohypoparathyroidism). In addi- hibition of renal reabsorption due to closure
tion, vitamin D deficiency can lead to hypocal- of tight junctions and activation of the Ca 2+ re-
cemia via a diminished formation of calcitriol. ceptor), increased thirst with polydipsia, and
In renal failure phosphate elimination by the psychogenic disorders (→ A5). If present for
kidney is reduced, the plasma phosphate level long, nephrolithiasis may result. If total plasma
rises, and calcium phosphate is deposited in Ca 2+ concentration is above 3.5 mmol/L (so-
the body (→ p.110). One of the consequences called hypercalcemia syndrome), coma, cardi-
is hypocalcemia. Mg 2+ deficiency also leads to ac arrhythmias, and renal failure (mainly due
hypocalcemia, especially if there is no stimula- to Ca 2+ deposition in renal tissue) occur. An
tion of PTH release. important indication of the presence of hyper-
Even when the total Ca 2+ concentration in calcemia syndrome is precipitation of calcium
blood is normal, the concentration of the effec- phosphate in the locally alkaline cornea
tive ionized Ca 2+ may be reduced because of (through loss of CO 2 ; cataract; “keratitis”). In
increased formation of complexes with proteins the ECG the ST segment is shortened in line
(in alkalosis), bicarbonate (in metabolic alka- with accelerated activation of the repolarizing
+
losis), phosphate (in renal failure, see above), K channels. Of great clinical significance in
and fatty acids (in acute pancreatitis; hypercalcemia is the increased sensitivity of
→ p.126, 158) (→ A3). the heart to digitalis, as this effect is normally
Hypercalcemia (→ A2) occurs in hyperpara- mediated via an increased cytosolic Ca 2+ con-
thyroidism and vitamin D excess. Malignant tu- centration (→ p.182).
128 mors with bone metastases lead to an in-
creased mobilization of calcium phosphate
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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