Page 26 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Effects of Tumors
If uncontrolled cell division occurs (→ p.14), The energy requirement of the tumor cells
cells undergo increasing dedifferentiation. If is frequently met by anaerobic glycolysis, even
this happens, the changed cells are often rec- if the O 2 supply is adequate, although the ener-
ognized and eliminated by the immune sys- gy yield per mol glucose is only 5% of the oxi-
tem. Tumor cells can escape this development dative glucose breakdown. The result is hypo-
by, for example, expressing the ligand for the glycemia and acidosis (→ B). The hypoglycemia
CD95 receptor (→ A1) on their surface and stimulates the release of glucagon, epineph-
thus driving the lymphocytes to apoptosis rine, and glucocorticoids that promote the
(→ p.12). A compromized immune response breakdown of fat and protein. Ultimately, pa-
(e.g., HIV infection; → p. 58) also helps tumor tients will lose weight (tumor cachexia; → B).
cells to survive. Sometimes tumor cells can activate hemosta-
If the tumor cell proliferates, a tumor devel- sis and/or fibrinolysis so that blood clotting or
ops that may have severe consequences blood loss may occur. Hemorrhage, the high
through its local extension alone. Thus, a brain iron requirement of tumor cells and tumor ca-
tumor can displace neighboring neurons and
chexia commonly lead to anemia (→ p. 38).
Fundamentals may thus cause, for example, epilepsy (→ A2 marked increase of tissue-specific activities, or
Tumors often cause abnormalities by a
and p. 338). As the bony nature of the cranium
by taking on new, non-tissue-specific activ-
prevents any significant increase in brain vol-
ities. Thus, plasma-cell tumors frequently
ume, a brain tumor ultimately leads to a life-
that damage organs, for example, the kidneys
(→ p. 358). Abronchial carcinomacan interrupt
1 threatening increase in intracranial pressure form large amounts of abnormal antibodies
the supply of air to the related alveoli and thus (→ p.102). Through their dedifferentiation, tu-
provoke their collapse (atelectasis; → p. 72). mor cells also express proteins, against which
Markedly dedifferentiated tumors gain the antibodies can be formed. Antibodies that
capacity to migrate to other tissues (metasta- have been formed by or against tumor cells
sis; → A3). For this to occur, the tumor cell can, among other effects, block ionic channels
must free itself from the bonds to its neigh- and receptors and thus for example cause
bour cells, intrude into blood vessels, leave myasthenia (→ p. 304).
the bloodstream on reaching another organ, Even small tumors of endocrine tissues and
and form new colonies there. Leaving the orig- dedifferentiated tumors of non-endocrine tis-
inal site of the cell requires the ability to mi- sues (in particular small-cell bronchial carci-
grate, and the breakdown of tissue boundaries. noma) frequently cause massive hormonal ab-
The latter is achieved by releasing proteolytic normalities (→ B). The increased release of hor-
enzymes, or by suppressing expression or ac- mones can result in numerous abnormalities
tion of proteinase inhibitors. Once the tumor (→ chap. 9), for example, raised blood pressure,
cells have entered a blood vessel they get stuck hypotonic hyperhydration, catabolism, acro-
in the next capillary. To leave the bloodstream megaly, hypoglycemia, bone breakdown, hy-
they must dock onto specific adhesion mole- percalcemia and renal stones, polycythemia,
cules of the endothelium and break through hyperthyroidism, virilization, galactorrhea,
the vessel wall. diarrhea, and peptic ulcers. On the other hand,
The increase in size of the tumor or its hormones are used as diagnostic tumor mark-
metastases requires the appropriate capillari- ers, e.g. calcitonin (medullary thyroid carcino-
ma), choriongonadotropin (testicular carcino-
zation, so that the tumor is supplied with O 2
and substrates. Angiogenesis is stimulated ma among others) and ACTH (lung tumors).
through the release of mediators and can be Death of tumor cells, through the release of
+
inhibited by angiogenesis inhibitors (e.g. an- cellular K , results in hyperkalemia, and the
giostatin, endostatin). If the tumor is very breakdown of nucleic acid leads to hyperurice-
large, the necessary additional blood flow mia (→ B and p. 250).
16 through the tumor increases the circulatory
load (cardiac output ↑; → B).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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