Dyspepsia (cont.)
What causes dyspepsia (indigestion)?
It's not surprising that many gastrointestinal diseases have been
associated with dyspepsia. However, many non-gastrointestinal diseases also have
been associated with dyspepsia. Examples of the latter include
diabetes, thyroid
disease, hyperparathyroidism (overactive parathyroid glands), and severe kidney
disease. It is not clear, however, how these non-gastrointestinal diseases
might cause dyspepsia. A second important cause of dyspepsia is drugs. It
turns out that many drugs are frequently associated with dyspepsia, for example,
nonsteroidal anti-inflammatory drugs (NSAIDs such as ibuprofen), antibiotics,
and estrogens). In fact, most drugs are reported to cause dyspepsia in at least
some patients.
As discussed previously, most dyspepsia (not due to
non-gastrointestinal diseases or drugs) is believed to be due to abnormal
function (dysfunction) of the muscles of the organs of the gastrointestinal
tract or the nerves controlling the organs. The nervous control of the
gastrointestinal tract, however, is complex. A system of nerves runs the entire
length of the gastrointestinal tract from the esophagus to the anus in the
muscular walls of the organs. These nerves communicate with other nerves that
travel to and from the spinal cord. Nerves within the spinal cord, in turn,
travel to and from the brain. (The gastrointestinal tract is exceeded in the
numbers of nerves it contains only by the spinal cord and brain.) Thus, abnormal
function of the nervous system in dyspepsia might occur in a gastrointestinal
muscular organ, the spinal cord, or the brain.
The nervous system controlling the gastrointestinal organs, as with most
other organs, contains both sensory and motor nerves. The sensory nerves
continuously sense what is happening (activity) within the organ and relay this
information to nerves in the organ's wall. From there, information can be
relayed to the spinal cord and brain. The information is received and processed
in the organ's wall, the spinal cord, or the brain. Then, based on this
sensory input and the way the input is processed, commands (responses) are sent
to the organ over the motor nerves. Two of the most common motor responses in
the intestine are contraction or relaxation of the muscle of the organ and
secretion of fluid and/or mucus into the organ.
As already mentioned, abnormal function of the nerves of the gastrointestinal
organs, at least theoretically, might occur in the organ, spinal cord, or brain.
Moreover, the abnormalities might occur in the sensory nerves, the motor nerves,
or at processing centers in the intestine, spinal cord, or brain.
Some researchers argue that the cause of functional diseases is
abnormalities in the function of sensory nerves. For example, normal activities, such
as stretching of the small intestine by food, may give rise to sensory
signals that are sent to the spinal cord and brain, where they are perceived as
painful. Other researchers argue that the cause of functional diseases is
abnormalities in the function of motor nerves. For example, abnormal commands
through the motor nerves might produce painful spasm (contraction) of the
muscles. Still others argue that abnormally functioning processing centers are
responsible for functional diseases because they misinterpret normal sensations
or send abnormal commands to the organ. In fact, some functional diseases may be
due to sensory dysfunction, motor dysfunction, or both sensory and motor
dysfunction. Others may be due to abnormalities within the processing centers.
An important concept that is relevant to these several potential mechanisms
(causes) of functional diseases is the concept of "visceral hypersensitivity". This concept
states that diseases affecting the gastrointestinal organs (viscera) "sensitize"
(alter the responsiveness of) the sensory nerves or the processing centers to
sensations coming from the organ. According to this theory, a disease such as
colitis (inflammation of the colon) can cause permanent changes in the
sensitivity of the nerves or processing centers of the colon. As a result of
this prior inflammation, normal stimuli are perceived (felt) as abnormal (for
example, as being painful). Thus, a normal colonic contraction may be painful.
It is not clear what prior diseases might lead to hypersensitivity in people,
although infectious diseases (bacterial or viral) of the gastrointestinal tract
are mentioned most often. Visceral hypersensitivity has been demonstrated
clearly in animals and people. Its role in the common functional diseases,
however, is unclear.
Another potential cause of dyspepsia is bacterial overgrowth of the small
intestine (small intestinal
bacterial overgrowth), although the frequency with which this condition
causes dyspepsia has not been determined, and there is little research in the
area. The relationship between overgrowth and dyspepsia needs to be
persued, however, since many of the symptoms of dyspepsia are also symptoms
of bacterial overgrowth. Overgrowth can be diagnosed by hydrogen breath testing
and is treated primarily with antibiotics.
Other diseases and conditions can aggravate functional diseases, including
dyspepsia. Anxiety and/or depression are probably the most commonly-recognized
exacerbating factors for patients with functional diseases. Another aggravating
factor is the menstrual cycle. During their periods, women often note that their
functional symptoms are worse. This corresponds to the time during which the
female hormones, estrogen and progesterone, are at their highest levels.
Furthermore, it has been observed that treating women who have dyspepsia with
leuprolide (Lupron),
an injectable drug that shuts off the body's production of estrogen and
progesterone, is effective at reducing symptoms of dyspepsia in premenopausal
women. These observations support a role for hormones in the intensification of
functional symptoms.
Next: What is the course of dyspepsia (indigestion)? »
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