Download THE GASTROINTESTINAL SYSTEM

THE GASTROINTESTINAL SYSTEM.
The gastrointestinal (GI) system has the critical task of supplying essential nutrients to fuel all the
physiologic and pathophysiologic activities of the body. Its functioning profoundly affects the quality
of life through its impact on overall health. The GI system has two major components: the alimentary
canal, or GI tract, and the accessory organs. A malfunction anywhere in the system can produce farreaching metabolic effects, eventually threatening life itself.
The alimentary canal is a hollow muscular tube that begins in the mouth and ends at the anus. It
includes the oral cavity, pharynx, esophagus, stomach, small intestine, and large intestine. Peristalsis
propels the ingested material along the tract; sphincters prevent its reflux. Accessory glands and
organs include the salivary glands, liver, biliary duct system (gallbladder and bile ducts), and
pancreas.
Together, the GI tract and accessory organs serve two major functions: digestion (breaking down
food and fluids into simple chemicals that can be absorbed into the bloodstream and transported
throughout the body) and elimination of waste products from the body through defecation.
PATHOPHYSIOLOGIC CONCEPTS
Disorders of the GI system often manifest as vague, nonspecific complaints or problems that
reflect disruption in one or more of the system's functions. For example, movement through the GI
tract can be slowed, accelerated, or blocked, and secretion, absorption, or motility can be altered. As
a result, one patient may present with several problems, the most common being anorexia,
constipation, diarrhea, dysphagia, jaundice, nausea, and vomiting. Based on the type of physiologic
process which is deranged disorders of digestion can be classified into following forms:
– disorders of appetite;
– disorders of secretion;
– disorders of absorption;
– disorders of motility.
DISORDERS OF APPETITE
1) Hyporexia, anorexia.
2) Fast satiety means rapid loss of appetite soon after beginning of eating. This disorder may
be observed after resection of the stomach and in certain mental conditions.
3) Hyperrexia (bulimia) may occur in some endocrine disorders (e.g. diabetes mellitus), some
mental disorders (schizophrenia, bulimia neurosa).
4) Parorexia implies eating of uneatable substances. It may occur in schizophrenia, irondeficient anemia.
Anorexia
Anorexia is a loss of appetite or a lack of desire for food. Nausea, abdominal pain, and diarrhea
may accompany it. Anorexia can result from dysfunction, such as cancer, heart disease, or renal
disease, in the gastrointestinal system or other systems.
Normally, a physiologic stimulus is responsible for the sensation of hunger. Falling blood glucose
levels stimulate the hunger center in the hypothalamus; rising blood fat and amino acid levels
promote satiety. Hunger is also stimulated by contraction of an empty stomach and suppressed when
the GI tract becomes distended, possibly as a result of stimulation of the vagus nerve. Sight, touch,
and smell play subtle roles in controlling the appetite center.
In anorexia, the physiologic stimuli are present but the person has no appetite or desire to eat.
Slow gastric emptying or gastric stasis can cause anorexia. High levels of neurotransmitters such as
serotonin (may contribute satiety) and excess cortisol levels (may suppress hypothalamic control of
hunger) have been implicated.
DISORDERS OF DIGESTION IN THE ORAL CAVITY.
Dysfunction of the salivary glands.
Hypersalivation.
Hypersalivation occurs in stomatitis, intoxication by nicotine or mercury, toxicosis of pregnancy,
parasitic infection, drugs increasing the vagal tone (m-cholinomimetics) or as a result of reflexes
(injury of the teeth or trigeminal nerve), disorders of the nervous system (encephalitis).
Hypersalivation leads to neutralization of the gastric juice, abnormal digestion of proteins, increased
passage of food to the duodenum.
Hyposalivation.
This may occur during inflammation or atrophy of the salivary glands, obstruction of the salivary
ducts, ingestion of drugs (cholinoblockers), some endocrine disorders, hypohydration, trauma or
infection of the brain.
DISORDERS OF ESOPHAGUS.
Disorders of motor function of the esophagus manifest as dysphagia.
Dysphagia.
Dysphagia — difficulty swallowing — can be caused by a mechanical obstruction of the
esophagus or by impaired esophageal motility secondary to another disorder. Dysphagia caused by a
large bolus or luminal narrowing is called mechanical dysphagia, whereas dysphagia due to
incoordination or weakness of peristaltic contractions or to impaired deglutitive inhibition is called
motor dysphagia.
Mechanical obstruction is characterized as intrinsic or extrinsic.
Intrinsic obstructions originate in the esophagus itself. Causes of intrinsic tumors include tumors,
strictures, and diverticular herniations. Extrinsic obstructions originate outside of the esophagus and
narrow the lumen by exerting pressure on the esophageal wall. Most extrinsic obstruction results
from a tumor.
The important causes of motor dysphagia are pharyngeal paralysis, cricopharyngeal achalasia,
scleroderma of the esophagus, achalasia, and diffuse esophageal spasm and related motor disorders.
Diffuse esophageal spasm is a motor disorder of the esophageal smooth muscle characterized by
multiple spontaneous contractions and by swallow-induced contractions that are of simultaneous
onset .
Distention and spasm at the site of the obstruction during swallowing may cause pain. Upper
esophageal obstruction causes pain 2 to 4 seconds after swallowing; lower esophageal obstructions,
10 to 15 seconds after swallowing. If a tumor is present, dysphagia begins with difficulty swallowing
solids and eventually progresses to difficulty swallowing semi-solids and liquids. Impaired motor
function makes both liquids and solids difficult to swallow.
Dysphagia is defined as a sensation of "sticking" or obstruction of the passage of food through the
mouth, pharynx, or esophagus..
WHAT HAPPENS IN SWALLOWING Before peristalsis can begin, the neural pattern to initiate
swallowing, illustrated here, must occur:
Food reaching the back of the mouth stimulates swallowing receptors that surround the pharyngeal
opening.
The receptors transmit impulses to the brain by way of the sensory portions of the trigeminal (V)
and glossopharyngeal (IX) nerves.
The brain's swallowing center relays motor impulses to the esophagus by way of the trigeminal
(V), glossopharyngeal (IX), vagus (X), and hypoglossal (XII) nerves.
Swallowing occurs.
Achalasia is a motor disorder of the esophageal smooth muscle in which the LES (lower
esophageal sphincter) does not relax properly with swallowing, and the normal peristalsis of the
esophageal body is replaced by abnormal contractions In achalasia, the esophageal ganglionic cells
are thought to have degenerated, and the cardiac sphincter of the stomach cannot relax. The lower end
of the esophagus loses neuromuscular coordination and muscle tone, and food accumulates, causing
hypertrophy and dilation.
Eventually, accumulated food raises the hydrostatic pressure and forces the sphincter open, and
small amounts of food slowly move into the stomach.
DYSFUNCTION OF THE STOMACH
Disorders of the secretory function:
Hypersecretion
Hypersecretion may be caused by:
1) Acute inflammation of the gastric mucosa with hyperplasia of the glandular epithelium
and/or increased histamine release:
– infection (H.pylori, Salmonella);
– spicy or coarse food;
– alcohol.
2) Excessive production of gastrin (Zollinger-Ellison syndrome).
3) Increased vagal tone:
– inadequate regulation due to psychological stress;
– ingestion of cholinomimetics.
4) Use of NSAID (aspirin).
5) Endocrine disorders: hyperthyroidism, Cushing's syndrome.
Hyposecretion
Causes of hyposecretion:
1) Chronic inflammation with atrophy of the gastric glands:
– e.g., due to autoimmune damage (pernicious anemia).
2) Abnormal regeneration of the mucosal epithelia:
– use of cytostatic drugs;
– B12 and folic acid deficiency;
– radiation damage.
3) Subtotal resection of the stomach, gastric cancer.
4) Decreased vagal tone:
– peripheral neuropathy due to diabetes mellitus);
– use of cholinoblockers;
– abnormal regulation.
5) Endocrine disorders: hypothyroidism, adrenal insufficiency, total pituitary insufficiency.
DISORDERS OF MOTOR FUNCTION
Disorders of motor function can take the form of hypotonia, hypertonia, hyperkinesia,
hypokinesia.
Hypotonia.
Acute hypotonia of the stomach may be caused by disorders of the neuromuscular, visceral
reflexes, overeating. In this condition the stomach may lose ability to propel food. Chronic hypotonia
may be caused by progressive deterioration of food evacuation (pylorospasm, ulcer of the antrum) or
a decrease in the contractile ability resulting from degeneration of the smooth muscles or fibrosis.
Hypertonia.
Hypertonia is often accompanied by increased peristalsis of the stomach. The underlying
mechanism includes a decreased excitability threshold of the autonomous nervous system with
enhanced vagal tone. The causative agents are intoxication by lead and zinc, vitamin B1 deficit (at
early stages), hyperacidic gastritis, neurosis.
Spastic contraction of the stomach delay passage of food to the lower parts of the gastrointestinal
tract.
Constipation.
Constipation is hard stools and difficult or infrequent defecation, as defined by a decrease in the
number of stools. Causes of constipation include dehydration, consumption of a low bulk diet, a
sedentary lifestyle, lack of regular exercise, and frequent repression of the urge to defecate.
When a person is dehydrated or delays defecation, more fluid is absorbed from the intestine, the
stool becomes harder, and constipation ensues. High fiber diets cause water to be drawn into the stool
by osmosis, thereby keeping stool soft and encouraging movement through the intestine. High fiber
diets also causes intestinal dilation, which stimulates peristalsis. Conversely, a low fiber diet would
contribute to constipation.
AGE ALERT The elderly typically experience a decrease in intestinal motility in addition to a
slowing and dulling of neural impulses in the GI tract. Many older persons restrict fluid intake to
prevent waking at night to use the bathroom or because of a fear of incontinence. This places them at
risk for dehydration and constipation.
A sedentary lifestyle or lack of exercise can cause constipation because exercise stimulates the
gastrointestinal tract and promotes defecation. Antacids, opiates, and other drugs that inhibit bowel
motility also lead to constipation.
Stress stimulates the sympathetic nervous system, and GI motility slows. Absence or degeneration
in the neural pathways of the large intestine also contributes to constipation. And other conditions,
such as spinal cord trauma, multiple sclerosis, intestinal neoplasms, and hypothyroidism, can cause
constipation.
Diarrhea
Diarrhea is an increase in the fluidity or volume of feces and the frequency of defecation. Factors
that affect stool volume and consistency include water content of the colon and the presence of
unabsorbed food, unabsorbable material, and intestinal secretions. Large-volume diarrhea is usually
the result of an excessive amount of water, secretions, or both in the intestines. Small-volume
diarrhea is usually caused by excessive intestinal motility. Diarrhea may also be caused by a
parasympathetic stimulation of the gut initiated by psychological factors such as fear or stress.
The three major mechanisms of diarrhea are osmosis, secretion, and motility:
Osmotic diarrhea: The presence of nonabsorbable substance, such as synthetic sugar, or increased
numbers of osmotic particles in the intestine, increases osmotic pressure and draws excess water into
the intestine, thereby increasing the weight and volume of the stool.
Secretory diarrhea: A pathogen or tumor irritates the muscle and mucosal layers of the intestine.
The consequent increase in motility and secretions (water, electrolytes, and mucus) results in
diarrhea.
Motility diarrhea: Inflammation, neuropathy, or obstruction causes a reflex increase in intestinal
motility that may expel the irritant or clear the obstruction.
GASTRITIS
Chronic gastritis is inflammation of the gastric mucosa
Classification
1. Acute erosive . (Acute hemorrhagic) gastritis is acute inflammation, erosion, and hemorrhage
of the gastric mucosa due to a breakdown of the mucosal barrier and acid-induced injury. It is caused
by the overuse of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, and alcohol
smoking, chemotherapy
2. Chronic gastritis Chronic gastritis is chronic inflammation of the gastric mucosa resulting in
eventual atrophy (chronic atrophic gastritis)
a. Type A gastritis is caused by autoantibodies against parietal cells, resulting in destruction of the
glands that secrete hydrochloric acid and intrinsic factor. The lack of intrinsic factor hinders
absorption of vitamin B12, leading to pernicious anemia.
b. Type B gastritis is caused by Helicobacter pylori infection.
3. Hypertrophic gastritis includes several conditions, such as Menetrier disease, which is
idiopathic, and hypergastrinemia, which is caused by endocrine tumors in patients with ZollingerEllison syndrome. Zollinger-Ellison syndrome are caused pancreatic gastrinoma producing gastrin,
which increases acid secretion and result in multiple intractable peptic ulcers
Autoimmune Gastritis.
This form of gastritis accounts for less than 10% of cases of chronic gastritis. It results from the
presence of autoantibodies to components of gastric gland parietal cells, including antibodies against
the acidproducing enzyme H+ ,K+ -ATPase, gastrin receptor, and intrinsic factor. Gland destruction
and mucosal atrophy lead to loss of acid production. In the most severe cases, production of intrinsic
factor is lost, leading to pernicious anemia. This uncommon form of gastritis is seen in association
with other autoimmune disorders such as Hashimotothyroiditis, Addison disease, and type 1 diabetes.
Patients with autoimmune gastritis have a significant risk for developing gastric carcinoma and
endocrine tumors (carcinoid tumor).
Chronic gastritis may affect different regions of the stomach and exhibit varying degrees of
mucosal damage. Autoimmune gastritis is characterized by diffuse mucosal damage of the bodyfundic mucosa, with less intense to absent antral damage, probably due to the autoantibodies against
parietal cells. Gastritis in the setting of environmental etiologies (including infection by H. pylori)
tends to affect antral mucosa or both antral and body-fundic mucosa (pangastritis). The mucosa is
usually reddened and has a coarser texture than normal. The inflammatory infiltrate may create a
mucosa with thickened rugal folds, mimicking early infiltrative lesions. Alternatively, with longstanding atrophic disease, the mucosa may become thinned and flattened. Irrespective of cause or
location, the histologic changes are similar. "Active" inflammation is signified by the presence of
neutrophils within the glandular and surface epithelial layer. Active inflammation may be prominent
or absent.
Lymphoid aggregates, some with germinal centers, are frequently observed within the mucosa.
Several additional histologic features are characteristic: •
Regenerative Change. A proliferative response to the epithelial injury is a constant feature of
chronic gastritis.
Metaplasia. The antral, body, and fundic mucosa may become partially replaced by metaplastic
columnar absorptive cells and goblet cells of intestinal morphology (intestinal metaplasia), both along
the surface epithelium and in rudimentary glands. Occasionally, villus-like projections may appear.
Atrophy. Atrophic change is evident by marked loss in glandular structures. Atrophy is quite
frequently associated with autoimmune gastritis and pangastritis caused by H.pylori.
A particular feature of atrophic gastritis of autoimmune origin or chronic gastritis treated by
inhibitors of acid secretion is hyperplasia of gastrin-producing G-cells in the antral mucosa. This is
attributed to the hypochlorhydria or achlorhydria arising from severe parietal cell loss. The G-cell
hyperplasia is responsible for the increased gastrinemia, which stimulates hyperplasia of
enterochromaffin-like cells in the gastric body.
• Dysplasia. With long-standing chronic gastritis, the epithelium develops cytologic alterations,
including variation in size, shape, and orientation of epithelial cells, and nuclear enlargement and
atypia. Intestinal metaplasia may precede the development of dysplasia. Dysplastic alterations may
become so severe as to constitute in situ carcinoma. The development of dysplasia is thought to be a
precursor lesion of gastric cancer in atrophic forms of gastritis, particularly in association with
pernicious anemia (autoimmune gastritis) and H. pylori- associated chronic gastritis.
ULCERS.
A gastrointestinal lesion is not necessarily an ulcer. Lesions that don't extend below the mucosal
lining (epithelium) are called erosions. Ulcers may be acute or chronic in nature. Lesions of both
acute and chronic ulcers can extend through the epithelium and perforate the stomach wall. Chronic
ulcers also have scar tissue at the base. Although erosions are often referred to as ulcers, erosions are
breaks in the mucosal membranes that do not extend below the epithelium.
Ulcers of the stomach and the duodenum may be manifestation of peptic ulcer disease or
symptomatic ulcers. Symptomatic ulcers are secondary ulcer damage of the stomach and the
duodenum which are connected with other disease or influence of the certain etiological factor.
Symptomatic ulcers are "stressful", medicinal, endocrine ulcers, and also the ulcers developing at
some diseases of internal bodies.
Gastric stress ulcers. multiple, small, round, superficial ulcers of the stomach. They arise at severe
stress. The causes of the ulcers may be shock, severe burns or trauma
Salicylates and other NSAIDs inhibit the secretion of prostaglandins (substances that block
ulceration). Certain illnesses, such as pancreatitis, hepatic disease, Crohn's disease, preexisting
gastritis, and Zollinger-Ellison syndrome, also contribute to ulceration.
PEPTIC ULCERS
Peptic ulcer disease is characterized by mucosal defects and deeper ulcerations in the stomach or
duodenum caused by gastric secretions (hydrochloric acid and pepsin) and impaired mucosal
defenses
Peptic ulcers, circumscribed lesions in the mucosal membrane extending below the epithelium,
can develop in the lower esophagus, stomach, pylorus, duodenum, or jejunum.
Gastric ulcers are most common in middle-aged and elderly men, especially in chronic users of
nonsteroidal anti-inflammatory drugs, alcohol, or tobacco. About 80% of all peptic ulcers are
duodenal ulcers, which affect the proximal part of the small intestine and occur most commonly in
men between ages 20 and 50. Duodenal ulcers usually follow a chronic course with remissions and
exacerbations; 5% to 10% of patients develop complications that necessitate surgery.
Causes and conditions
Peptic ulcers can result from factors that increase gastric acid production (hypersecretory
disorders) or from factors that impair mucosal barrier protection. Peptic ulcer's main causes, several
predisposing factors are acknowledged. They include blood type (gastric ulcers and type A; duodenal
ulcers and type O) and other genetic factors. Exposure to irritants, such as alcohol, coffee, and
tobacco, may contribute by accelerating gastric acid emptying and promoting mucosal breakdown.
Emotional stress also contributes to ulcer formation because of the increased stimulation of acid and
pepsin secretion and decreased mucosal defense. Physical trauma and normal aging are additional
predisposing conditions.
Pathophysiology
Although the stomach contains acidic secretions that can digest substances, intrinsic defenses
protect the gastric mucosal membrane from injury. A thick, tenacious layer of gastric mucus protects
the stomach from autodigestion, mechanical trauma, and chemical trauma. Prostaglandins provide
another line of defense. Gastric ulcers may be a result of destruction of the mucosal barrier.
The duodenum is protected from ulceration by the function of Brunner's glands. These glands
produce a viscid, mucoid, alkaline secretion that neutralizes the acid chyme. Duodenal ulcers appear
to result from excessive acid protection. The bacteria Helicobacter pylori are a contributing factor in
chronic gastritis (chronic inflammation of stomach mucosa) and in ulcer formation. They're typically
seen within the muscular layers and between cells that line the gastric pits. These bacteria cause
tissue inflammation, which can lead to ulcers. Helicobacter pylori releases a toxin that destroys the
gastric and duodenal mucosa, reducing the epithelium's resistance to acid digestion and causing
gastritis and ulcer disease.
Signs and symptoms
Symptoms vary by the type of ulcer.
A gastric ulcer produces the following signs and symptoms: pain that worsens with eating due to
stretching of the mucosa by food; nausea and anorexia secondary to mucosal stretching.
A duodenal ulcer produces the following signs and symptoms: epigastric pain that is gnawing,
dull, aching, or “hunger like” due to excessive acid production; pain relieved by food or antacids, but
usually recurring 2 to 4 hours later secondary to food acting as a buffer for acid.
Healing of ulcers
In the absence of an effective mucous barrier, an irritant can cause the basal lamina to exfoliate or
slough off. A process called rapid reepithelialization, shown below, replenishes the damaged
epithelium and repairs any defects.
Complications
Hemorrhage, shock, gastric perforation, gastric outlet obstruction.
Diagnosis
Barium swallow or upper GI and small bowel series may reveal the presence of the ulcer. This is
the first test performed on a patient when symptoms aren't severe. Endenoscopy confirms the
presence of an ulcer and permits cytologic studies and biopsy to rule out H. pylori or cancer.
Upper GI tract X-rays reveal mucosal abnormalities. Stool analysis may reveal occult blood.
Serologic testing may disclose clinical signs of infection, such as elevated white blood cell count.
Gastric secretory studies show hyperchlorhydria. Carbon13 urea breath test results reflect activity
of H. pylori.
Treatment
Dietary therapy with small infrequent meals and avoidance of eating before bedtime to neutralize
gastric contents, avoidance of caffeine and alcohol to avoid stimulation of gastric acid secretion
Eradicate H. pylori infection
Inhibit gastric acid secretion and increase carbonate and mucus production, to protect the stomach
lining
Antacids to neutralize acid gastric contents by elevating the gastric pH, thus protecting the mucosa
and relieving pain
Sucralfate, mucosal protectant to form an acid-impermeable membrane that adheres to the mucous
membrane and also accelerates mucus production
Surgery to repair perforation or treat unresponsiveness to conservative treatment, and suspected
malignancy.
ENTERITIS
Enteritis is inflammation of the small intestine associated with diarrhea, malabsorption or both.
1. Infectious causes
a. Viruses (e.g., rotavirus, Norwalk virus), most common in children
b. Bacteria
(1) Escherichia coli (food-borne)
(2) Vibrio cholerae (water-borne)
(8) Staphylococcus aureus, which secretes a preformed toxin and causes "food poisoning"
(4) Mycobacterium avium-intracellulare (MAI), which can cause enteritis in patients with AIDS
(5)Tropheryma whippelii, the intracellular bacterium responsible for Whipple disease (a
malabsorption syndrome)
e. Parasites (e.g., lamblia)
2. Celiac sprue. Gluten intolerance leads to atrophy of the intestinal villi and, consequently,
malabsorption.
MALABSORPTION
Malabsorption is characterized by suboptimal absorption of fats, fat-soluble and other vitamins,
proteins, carbohydrates, electrolytes and minerals, and water.
Malabsorption is caused by:
1) abnormal intraluminal digestion;
2) abnormal terminal digestion;
3) accelerated transit of the intestinal chymus;
4) a decrease in the surface area of absorption;
5) a decrease in transepithelial transport, in which nutrients, fluid, and electrolytes are transported
across the epithelium of the small intestine for delivery to the intestinal vasculature.
Malabsorption is failure of the intestinal mucosa to absorb single or multiple nutrients efficiently.
Absorption of amino acids, fat, sugar, or vitamins may be impaired. The result is inadequate
movement of nutrients from the small intestine to the bloodstream or lymphatic system.
Manifestations depend primarily on what is not being absorbed.
Causes
A wide variety of disorders result in malabsorption. (See Causes of malabsorption.): prior gastric
surgery, pancreatic disorders, hepatobiliary disease, disease of the small intestine, hereditary
disorder, drug toxicity.
Pathophysiology
The small intestine's inability to absorb nutrients efficiently may result from a variety of disease
processes. The mechanism of malabsorption depends on the cause. Some common causes of
malabsorption syndrome include celiac disease, lactase deficiency, gastrectomy, Zollinger-Ellison
syndrome, and bacterial overgrowth in the duodenal stump.
In celiac sprue, dietary gluten — a product of wheat, barley, rye, and oats — is toxic to the
patient, causing injury to the mucosal villi. The mucosa appear flat and have lost absorptive surface.
Symptoms generally disappear when gluten is removed from the diet.
Lactase deficiency is a disaccharide deficiency syndrome. Lactase is an intestinal enzyme that
splits nonabsorbable lactose (a disaccharide) into the absorbable monosaccharides glucose and
galactose. Production may be deficient, or another intestinal disease may inhibit the enzyme.
Malabsorption may occur after gastrectomy. Poor mixing of chyme with gastric secretions is the
cause of postsurgical malabsorption.
In Zollinger-Ellison syndrome, increased acidity in the duodenum inhibits release of
cholecystokinin, which stimulates pancreatic enzyme secretion. Pancreatic enzyme deficiency leads
to decreased breakdown of nutrients and malabsorption. Bacterial overgrowth in the duodenal stump
(loop created in the Billroth II procedure) causes malabsorption of vitamin B12.
Signs and symptoms
Signs and symptoms include: weight loss and generalized malnutrition from impaired absorption
of carbohydrate, fat, and protein; diarrhea from decreased absorption of fluids, electrolytes, bile acids
and fatty acids in colon; steatorrhea from excess fat in stool; flatulence and abdominal distention
secondary to fermentation of undigested lactose; nocturia from delayed absorption of water;
weakness and fatigue from anemia and electrolyte depletion from diarrhea; edema from impaired
absorption of amino acids, resulting in protein depletion and hypoproteinemia; amenorrhea from
protein depletion leading to hypopituitarism; anemia from the impaired absorption of iron, folic acid,
and vitamin B12; glossitis, cheilosis secondary to a deficiency of iron, folic acid, vitamin B12, and
other vitamins; peripheral neuropathy from a deficiency of vitamin B12 and thiamine; bruising,
bleeding tendency from vitamin K malabsorption and hypoprothrombinemia; bone pain, skeletal
deformities, fractures from calcium malabsorption that leads to hypocalcemia; protein depletion
leading to osteoporosis and vitamin D malabsorption causing impaired calcium absorption; tetany,
paresthesias resulting from calcium malabsorption leading to hypocalcemia and magnesium
malabsorption, leading to hypomagnesemia and hypokalemia.
Diagnosis
Stool specimen for fat reveals excretion of greater than 6 g of fat per day.
D-Xylose absorption test shows less than 20% of 25 g of D-Xylose in the urine after 5 hours,
reflects disorders of proximal bowel.
Schilling test reveals deficiency of vitamin B12 absorption.
Culture of duodenal and jejunal contents confirms bacterial overgrowth in the proximal bowel.
Gastrointestinal barium studies show characteristic features of the small intestine.
Small intestine biopsy reveals the atrophy of mucosal villi.
Treatment
Identification of cause and appropriate correction
Gluten-free diet to stop progression of celiac disease and malabsorption
Lactose-free diet to treat lactase deficiency
Dietary supplementation to replace nutrient deficiencies
Vitamin B12 injections to treat vitamin B12deficiency.
CAUSES OF MALABSORPTION.
Many disorders — from systemic to organ-specific diseases — may give rise to malabsorption
Primary small bowel
disease
DISEASES OF THE SMALL INTESTINE
Tropical sprue
Bacterial overgrowth due to stasis in afferent loop after Billroth II
gastrectomy
Ischemic small bowel
disease
Small bowel infections
and infestations
Systemic disease
involving small bowel
Massive bowel resection
Nontropical sprue (celiac disease)
Regional enteritis
Chronic congestive heart failure
Mesenteric atherosclerosis
Acute enteritis
Giardiasis
Amyloidosis
Lymphoma
Sarcoidosis
Scleroderma
Whipple's disease
DRUG-INDUCED MALABSORPTION
Calcium carbonate
Neomycin
HEPATOBILIARY DISEASE
Biliary fistula
Biliary tract obstruction
Cirrhosis and hepatitis
HEREDITARY DISORDER
Primary lactase deficiency
PANCREATIC DISORDERS
Chronic pancreatitis
Cystic fibrosis
Pancreatic cancer
Pancreatic resection
Zollinger-Ellison syndrome
PREVIOUS GASTRIC SURGERY
Billroth II gastrectomy
Pyloroplasty
Total gastrectomy
Vagotomy
Complications
Fractures
Anemias
Bleeding disorders
Tetany
Malnutrition.