   
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Normal digestion and absorption of foods is essential for life and well-being. Given the length of the gastrointestinal tract, the number of organs involved in digestion, and the large number of nutrients that must be taken into our bodies, it is not surprising to find a large number of disease states that impair the processes of food digestion and absorption. Clinical malassimilation occurs in only one of two ways: (1) through intraluminal disorders (maldigestion of food) and (2) through intramural disorders (malabsorption of food).
The list of
diseases that can cause malassimilation is long (Table
3), necessitating logical history-taking.
Clinical suspicion, as always, comes from the patient's history and
physical examination. Pancreatic insufficiency Reduced intestinal bile salt
concentration A patient with
malassimilation may have symptoms and signs of specific nutrient
deficiencies or those of the underlying disease process itself (e.g.,
Crohn's disease). Furthermore, considering that malassimilation usually
involves multiple nutrients, the symptoms and signs of a malassimilation
state can vary from a straightforward presentation to myriad symptom
complexes (Table 4
and Table 5). The patient who gives a
history of progressive weight loss, polyphagia, excessive flatus,
diarrhea, bulky and foul-smelling stools, food particles or fat in the
stool, abdominal distention, muscle wasting, bone pain, bleeding,
weakness, tetany, paresthesia, glossitis, cheilosis or dermatitis is
giving you the "classical" history of severe intestinal
malassimilation. Rarely will you hear such a history from a patient in
North America. It is far more common to see patients who will have vague
symptoms for which there is some abnormality in their blood chemistry that
alerts you to the presence of disease.
Early symptoms of the disease may easily be overlooked,
and a severely malnourished state may come to exist. Often a patient will
have noticed "early" symptoms, which will become apparent only
when questioned directly. Hence, the physician must inquire about minor
changes in bowel habits occurring before the onset of weight loss,
hyperphagia, pain, anorexia or gross changes in bowel habits. Subtle
changes in stool volume or bulk (manifested by a slight increase in the
number of bowel movements per day), consistency or odor are early
manifestations of malassimilation. A slight increase in the frequency of
stools occurring at a time when the patient is mildly anorexic occurs a
long time before disease becomes clinically apparent. An early increase in
bulk of the stool is caused by increased water and gas content and leads
to an inability to flush the stool easily. It is not uncommon for the patient to think the toilet
is malfunctioning because several flushings are needed to remove the
stool. A greasy character and truly rancid odor are indicative of
increased stool fat, but are often absent until late. These complaints are
often readily passed over by the busy physician. At such time, physical
findings are usually absent, but hyperactive bowel sounds may be noted,
especially in small intestinal disease. If symptoms are intermittent or if
they progress slowly over many years, patients may exhibit vague,
seemingly unrelated symptoms such as chronic fatigue and depression, long
before the physician considers the possibility of serious organic disease. Carbohydrate
malassimilation will result in both specific and generalized symptoms.
Specific to the maldigestion and malabsorption of carbohydrates are
diarrhea and excess flatus. Unfortunately, everyone has flatus, and a
definition or measure of excessive "wind" is lacking.
Malabsorbed carbohydrates that enter the colon are fermented by colonic
bacteria to gases (CO2, H2 and CH4) and
organic acids (Figure 12).
These organic acids produce diarrhea by acting directly on colonic
epithelium to stimulate fluid secretion and by their osmotic effect, which
further draws water into the lumen. The presence of organic acids in the
stool reduces the pH below 6 and suggests carbohydrate malassimilation.
The gas produces flatulence, with associated borborygmi and abdominal
distention. The presence of intraluminal H2 gas, eventually
absorbed into the circulation and exhaled, forms the basis of the hydrogen
breath test to detect carbohydrate malabsorption. Physical examination
often reveals a distended tympanitic abdomen with hyperactive bowel
sounds. Stools seem to float on the water because of their increased gas
content (not because of their fat content).
Generally, lack of carbohydrate as an energy source
will result in decreased plasma insulin levels, increased plasma glucagon
and cortisol levels and decreased peripheral T4-to-T3
conversion. Given sufficient time, the body will enter a state of
oxidative metabolism: fat and muscle will be catabolized. Physical
examination may reveal signs of weight loss from both fat stores and lean
body mass. The patient will be weak and will easily develop fatigue. Fat
loss will generally be noted as sunken cheeks and flat buttocks, with
wrinkled or loose skin indicative of loss of subcutaneous fat stores. The
loss of muscle mass is easily noted as thenar mass reduction and sunken
soft tissues between the extensor tendons on the dorsum of the hands.
There may be direct evidence of a reduced metabolic rate secondary to
decreased T3 conversion. The patient will often be mentally
slowed. Failure to
digest or absorb fats results in a variety of clinical symptoms and
laboratory abnormalities. These manifestations are the result of both fat
malassimilation per se and a deficiency of the fat-soluble vitamins. In
general, loss of fat in the stool deprives the body of calories and
contributes to weight loss and malnutrition. More specific is the action
of unabsorbed long-chain fatty acids, which act on the colonic mucosa to
cause diarrhea by an irritant effect on the colon. In addition, fatty
acids bind calcium, which would normally be available to bind oxalate. In
fat malabsorption, oxalate is not bound to calcium and remains free (undissociated)
within the colonic lumen, where it is readily absorbed. This results in
oxaluria and calcium oxalate kidney stones. This occurs in Crohn's disease
more readily than in other cases of fat malabsorption (steatorrhea).
Failure to absorb the fat-soluble vitamins A, D, E and
K also results in a variety of symptoms. Vitamin K deficiency presents as
subcutaneous, urinary, nasal, vaginal and gastrointestinal bleeding.
Deficiencies in factors II, VII, IX and X produce defective coagulation.
Vitamin A deficiency results in follicular hyperkeratosis. Vitamin E
deficiency leads to a progressive demyelination of the central nervous
system. Malabsorption of vitamin D causes rickets and osteopenia, as
discussed later. Severe loss
of body protein may occur before the development of laboratory
abnormalities. Impaired protein synthesis from liver diseases and
excessive protein loss in renal disease can further aggravate protein
deficiencies. Clinically, protein deficiency results in edema and
diminished muscle mass. Since the immune system is dependent upon adequate
proteins, protein deficiency can manifest as recurrent or severe
infections. Protein deficiency in children results in growth retardation,
mental apathy and irritability, weakness and muscle atrophy, edema, hair
loss, deformity of skeletal bone, anorexia, vomiting and diarrhea.
Protein-calorie malnutrition is known as marasmus, whereas protein
malnutrition by itself is known as kwashiorkor. |
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
