Page 148 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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reflux volume. pH clearance is dependent on weight loss. Serious complications of achala-
the amount and buffering capacity of saliva. sia are esophagitis and pneumonia, caused by
! The wall of the esophagus contains epi- aspiration of esophageal contents (contain-
thelium with barrier properties. Of its 25– ing bacteria).
30 cell layers (→ E, right) it is particularly Hypomotility of the esophagus is caused
the stratum corneum (ca. 10 layers) located by factors that are the opposite of those de-
at the luminal aspect that is especially dense. scribed above. In scleroderma (→ D), an au-
This largely prevents the invasion of the toimmune disease, hypomotility in its early
harmful components of gastric juice (H + stages is due to neuronal defects that later
ions, pepsin, and sometimes bile salts). Addi- result in atrophy of the smooth muscles of
tionally, as in the gastric mucosa (→ p.144), the esophagus, so that peristalsis in the distal
+
H ions that have penetrated into the cells portion ultimately ceases altogether. Con-
Liver are very efficiently removed to the outside trary to achalasia, the lower sphincter pres-
+
+
(Na /H exchange carrier), and also a small
sure is reduced, so that gastroesophageal re-
Stomach, Intestines, of the esophagus are caused by abnormal flux of gastric juice into the esophagus is to
–
number of HCO 3 ions are secreted.
flux disease develops.
Gastroesophageal reflux disease (→ E). Re-
The most important functional disorders
some extent a physiological phenomenon
esophageal contraction (hypermotility or hy-
(see above); heart burn indicates reflux
pomotility, disordered coordination) or fail-
esophagitis. This can be caused by:
ure of the protective mechanisms to cope
ease).
lower esophageal sphincter (→ B, D);
– increased frequency of transient sphincter
Hypermotility may be caused by a thick-
6 with reflux (gastroesophageal reflux dis- – factors that diminish the pressure in the
ened muscular layer, an increased sensitivity opening (swallowing air, drinks contain-
of the muscle toward excitatory transmitters ing CO 2 );
(acetylcholine), or hormones (e.g., gastrin), – decreased volume clearance (abnormal
or a reduced sensitivity toward inhibitory distal esophageal peristalsis);
transmitters (e.g., VIP). Hypermotility may – slowed pH clearance, for example, due to
also be due to increased neuronal activity of decreased salivary flow (sleep, chronic
cholinergic neurones or diminished activity saliva deficiency [xerostomia]), or de-
of inhibitory NCNA neurones. The latter is creased buffering capacity of the saliva
true of achalasia (→ C). This is caused by a re- (smoking cigarettes);
duction in the number of intramural NCNA – hiatus hernia, in which the abdominal
neurones as well as diminished reactivity of part of the esophagus is displaced into
these neurones to preganglionically liber- the thorax, so that an important mecha-
ated acetylcholine. As a result of this disor- nism of sphincter closure, increased in-
der, patients with achalasia have a greatly tra-abdominal pressure, is absent;
elevated resting pressure in the lower esopha- – direct irritation and damage to the esoph-
geal sphincter, receptive relaxation sets in ageal mucosa, for example, by citrus fruits,
late and, most importantly, is too weak, so tomato-based foods, hot spices, high-
that during the reflex phase the pressure in proof alcohol, and nonsteroid anti-inflam-
the sphincter is markedly higher than that matory drugs (NSAIDs; → p.142).
in the stomach (→ C, bottom). As a result, The result of chronic esophageal reflux is
swallowed food collects in the esophagus, epithelial metaplasia (→ p. 4) in the distal
causing a pressure rise throughout and un- esophagus that, as a precancerous condition,
der certain circumstances leading to an enor- can develop into cancer.
mous dilation of the esophagus (→ C). Fur-
thermore, propagation of the peristaltic
wave ceases (see also A1,2 and C, right).
Thus, the symptoms of achalasia are dyspha-
138 gia (trouble swallowing), regurgitation of
food (not vomiting), retrosternal pain, and
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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