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.pdf
USMLE Step 2 CK
Note
Sclerosing cholangitis does not
correlate to disease activity.
l Internal Medicine
INFLAMMATORY BOWEL DISEASE
Inflammatory bowel disease (IBD) is a term comprising 2 disease entities: Crohn’s disease
(CD) and ulcerative colitis (UC). They can be discussed simultaneously because of the large
degree of overlap in terms of presentation, testing, and treatment.
• Both CD and UC are idiopathic disorders of the bowel associated with diarrhea,
bleeding, weight loss, fever, and abdominal pain.
• Both are most accurately diagnosed with endoscopy and sometimes with barium studies, “string sign” on small bowel follow through after barium meal in CD.
• Both are treated with anti-inflammatory medications, such as mesalamine, azathioprine, and 6-mercaptopurine (6MP).
• Steroids are used for acute exacerbations of both diseases.
Clinical Presentation. IBD presents with fever, diarrhea, weight loss, and, occasionally, abdominal pain and bleeding. The extraintestinal manifestations of IBD are episcleritis, scleritis and
iritis, sclerosing cholangitis, joint pains, and skin manifestations, such as pyoderma gangrenosum or erythema nodosum.
Crohn’s disease is more likely to be associated with a palpable abdominal mass because CD
has granulomas in the bowel wall that are transmural in nature. This can lead to the different
loops of bowel being inflamed and sticking together, forming a mass. The abdominal masses
of CD can be palpated and cause pain. CD is not necessarily continuous, and one hallmark of
the disorder is that there are “skip lesions,” or areas of normal tissue in between the areas of
disease.
UC is limited exclusively to the large bowel. It is exclusively a mucosal disease, and although
it can cause bleeding, it does not result in fistula formation. UC has no skip lesions, no fistula
formation, and no oral or perianal involvement. UC is more likely to cause bloody diarrhea.
Both forms of IBD can lead to colon cancer after 8–10 years of involvement of the colon. If
the CD does not result in colonic involvement, then it will not lead to cancer. Complications
of Crohn’s disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.
Diagnosis. IBD is diagnosed with endoscopy and sometimes with barium studies. (CD can result
in deficiency of vitamin B12, calcium, vitamin K, and iron because of malabsorption.) Anti–
Saccharomyces cerevisiae antibodies (ASCA) are associated with CD, and antineutrophil cytoplasmic antibody (ANCA) is associated with UC. If a patient is ASCA positive and ANCA negative,
he has a >90% chance of having CD. If the patient is ASCA negative and ANCA positive, he has a
>90% chance of having UC.
Prothrombin time may be prolonged in CD because of vitamin K malabsorption. Kidney
stones form more often in CD because the fat malabsorption results in a low calcium level
and an increased absorption of oxalate, which forms kidney stones.
Treatment. Mesalamine derivatives are the mainstay of therapy for IBD in all of its forms.
Pentasa is a form of mesalamine released in both the upper and lower bowel; hence, it is
used in CD. Asacol is a form of mesalamine released in the large bowel, and it is most useful for UC. Rowasa is used exclusively for rectal disease. Sulfasalazine was used in the past
for the same effect. The difficulty with sulfasalazine is that the high load of sulfa delivered
causes a number of adverse effects, such as rash, hemolysis, and allergic interstitial nephritis. Sulfasalazine also causes reversible infertility in men and leukopenia by its sulfapyridine
group.
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Acute exacerbations of IBD are treated with high-dose steroids. Budesonide is a form of steroid
that is ideal for IBD. It has a strong local effect when used orally, but is largely cleared by the
liver in a first-pass effect. This limits the amount of systemic toxicity. Azathioprine and 6-mercaptopurine are associated with drug-induced pancreatitis, but are still used on a long-term
basis to try to keep patients off steroids. Ciprofloxacin and metronidazole are used for CD in
those with perianal disease. Infliximab is used for CD in those who form fistulae or have disease
refractory to the other forms of therapy. There has been re-activation of tuberculosis with infliximab, and it is important to test for latent tuberculosis with a purified protein derivative (PPD)
prior to treatment. If the PPD is positive, then patients should receive isoniazid. The most common side effect of infliximab is arthralgias. Balsalazide and olsalazine are other forms of mesalamine that are only active in the colon and are used occasionally.
Surgery is curative in UC; almost 60% of patients will require surgery within 5 years after diagnosis due to refractory symptoms or severe disease. Surgery is not very effective in CD and disease
tends to reoccur at the site of anastomosis.
l Gastroenterology
DIARRHEA
Diarrhea is increased frequency or volume of stool per day; stool can also be defined as diarrhea if the number of stools per day is few, but their consistency is watery.
Pathogenesis. The most common causes of diarrhea are of an infectious, antibiotic-associated, or lactose-intolerance etiology or from irritable bowel or carcinoid syndrome.
Clinical Presentation. The patient is often hypotensive, febrile, and experiencing abdominal
pain.
Diagnosis. The first thing to do in the evaluation of diarrhea in terms of direct patient care is
to see if there is hypovolemia as defined as hypotension or orthostasis. This is more important
than determining the specific etiology because of the chance that the patient may die while
waiting for the results to come back.
Treatment. No matter the etiology, if the patient is hypotensive, febrile, and having abdominal pain, he or she should be admitted to the hospital and given IV fluids and antibiotics. The
presence of blood in the stool is especially serious and is probably the single strongest indication for the use of antibiotics, such as ciprofloxacin.
Infectious Diarrhea
For all patients, assume that new-onset diarrhea has an infectious etiology. After an infectious
cause is excluded, then the other possible causes can be systematically ruled out.
In general, to exclude infection, stool should be evaluated for the presence of white cells or
“fecal leukocytes,” as well as culture and ova and parasite examination. Clostridium difficile
toxin and stool Giardia-antigen testing are done when there are clues to these diagnoses in the
history.
Note
With management of diarrhea,
determine when to admit
the patient and when to use
IV fluids and antibiotics.
That is more important than
determining the precise
causative agent.
The most common causes of infectious diarrhea are Campylobacter and Salmonella, especially
in patients with sickle cell and achlorhydria. One can only make a definitive determination of
the etiology with a stool culture.
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Clinical presentation
Table 4-1. Clues to the Diagnosis of Infectious Diarrhea Prior to Results of Culture
Causative Agent Patient Symptoms or History Additional Comments
Bacillus cereus Ingestion of refried Chinese food and the
spores from Bacillus that it contains. Vomiting
is prominent. Blood is never present.
Campylobacter Reactive arthritis, Guillain-Barré syndrome Most common cause of bacterial gastroenteritis
Cryptosporidia,
Isospora
E. coli 0157:H7 Associated with the ingestion of contaminated
Giardia The ingestion of unfiltered water, as on a
Salmonella Ingestion of chicken and eggs, dairy products —
Scombroid Patients who ingest contaminated fish
Found in HIV-positive patients with
<100/mm3 CD4 cells
hamburger meat. The organism can release
a Shiga toxin, provoking hemolytic uremic
syndrome.
camping trip or in the mountains, or in
drinking fresh lake water. Giardia never
gives blood in the stool. There is abdominal
fullness, bloating, and gas.
experience vomiting, diarrhea, flushing, and
wheezing within minutes of eating it.
Short incubation period (1–6 hours)
—
Hemolytic uremic syndrome happens when
the organism dies; that is why antibiotics are
contraindicated. Platelet transfusions are also
contraindicated, even if the platelet count is low
because the new platelets may only make it worse.
Giardia can also simulate celiac disease in terms
of causing fat and vitamin malabsorption if it is
not eradicated.
Organisms invade, producing and then releasing
histamine into the flesh of fish, such as tuna,
mahi mahi, and mackerel.
Shigella, Yersinia No clues strong enough to point to the
etiology until the results of the stool culture
are known.
Vibrio
parahaemolyticus
Vibrio vulnificus Also in raw shellfish, but has a particularly
Viral Children in day-care centers; the absence of
Staphylococcus aureus Ingestion of dairy products, eggs, salads.
Ciguatera-toxin 2–6 hours after ingestion of large reef fish
Ingestion of raw shellfish, such as mussels,
oysters, and clams
high incidence in people with underlying liver
disease or disorders of iron metabolism. Also
associated with the development of skin bullae.
blood and white cells
Upper GI symptoms (nausea/vomiting)
predominate; rarely diarrhea.
(grouper, red snapper, and barracuda).
Also neurological symptoms → paresthesia,
weakness, and reversal of heat and cold.
Yersinia can mimic appendicitis. Also
common in people with iron overload, e.g.,
hemochromatosis.
Typically presents as severe systemic
gastroenteritis in patients with underlying disease
(esp. chronic liver disease)
Typically presents as severe systemic
gastroenteritis in patients with underlying disease
(esp. chronic liver disease)
No systemic manifestation
Short incubation period (1–6 hours)
—
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Diagnosis. Stool for fecal leukocytes is the most useful test that can be done immediately.
Fecal leukocytes are only found when there has been invasion of the intestinal mucosa, as in
dysentery, which is a bacterial infection of the bowel, producing diarrhea and bloody stool.
Invasive organisms need 24 to 36 hours to produce their effect and never give blood in the
stool within the first few hours of their ingestion. (The only exception is the protozoan
Entamoeba histolytica, which can give blood or white cells in stools.) The invasive organisms
are Salmonella, Shigella, Campylobacter, Vibrio parahaemolyticus, Yersinia, Escherichia coli, and
Vibrio vulnificus (think people drinking sea water). The most definitive test for these bacterial
organisms is a stool culture.
Cryptosporidiosis is diagnosed with a unique test, a modified acid-fast test. The routine ova
and parasite examination does not reliably detect cryptosporidiosis.
Giardia is best diagnosed with an ELISA stool antigen test. A single stool antigen test has 90%
sensitivity. Three stool ova and parasite examinations have only 80% sensitivity.
l Gastroenterology
Treatment. Most cases of food poisoning and infectious diarrhea will resolve spontaneously
and will not need specific antimicrobial therapy. Even when they cause severe disease, as
defined by high-volume stools with dehydration, antibiotics generally do not help. Antibiotics
are used if there is abdominal pain, blood in the stool, and fever. The decision to use antibiotics is always made prior to knowing the result of the stool culture, so the treatment is always
empiric and then modified when the culture results are known. The best empiric therapy for
infectious diarrhea is ciprofloxacin or the other fluoroquinolones ± metronidazole.
Scombroid poisoning is treated with antihistamines, such as diphenhydramine. Giardia is still
treated primarily with metronidazole. A newer agent for Giardia is tinidazole, which is effective in a single dose. Cryptosporidiosis is treated with nitazoxanide, although it has limited
efficacy. The truly effective therapy for cryptosporidiosis is to raise the CD4 count to >100/
mm3 with antiretrovirals. Nitazoxanide is superior to paromomycin for cryptosporidium.
There is no specific therapy for viral diarrhea. Patients are managed with fluid and electrolyte
support until the infection resolves.
Antibiotic-Associated and C. difficile-Associated Diarrhea
The term antibiotic-associated diarrhea (AAD) refers usually to a benign, self-limited diarrhea
following the use of antimicrobials. Typically, no pathogens are identified and the diarrhea is
caused by changes in the composition and function of the intestinal flora as well as increased
motility (as occurs with agents like erythromycin). Most patients respond to supportive measures and discontinuation of antibiotics.
Note
• TMP/SMX for Isopora
• Doxycycline for Vibrio
vulnificus
• Rifaximin for travelers’
diarrhea
Note
Prophylactic antibiotics for
traveler’s diarrhea is never a
correct approach.
On the other hand, Clostridium difficile diarrhea (C. diff) refers to a spectrum of diarrheal illnesses caused by the toxins produced by this organism, including severe colitis with or without
the presence of pseudomembranes. For exam purposes, this discussion will focus on C. diff.
Pathogenesis. Any antibiotic can lead to diarrhea with C. diff, although antibiotics that are
broad spectrum are more likely to do so. Clindamycin may have one of the highest frequencies
of association, as do fluoroquinolones and cephalosporins.
C. diff diarrhea is largely a nosocomial disease and is the most frequent cause of diarrhea in
hospitalized patients. Its occurrence in the outpatient setting, other than in patients confined
to nursing homes, is much less common. Recent meta-analysis suggests a significant association between C. difficile and the use of proton pump inhibitors.
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• Epidemiologic studies have shown that C. difficile is often isolated in hospital wards,
including the floors, door handles, and furniture, even weeks after patients with it have
been removed from the area.
• Because of the sporulating properties of this organism, all these observations have
suggested an important role for cross-contamination between patients, contact with
environmental surfaces, and transmission via hands of medical personnel.
• During the past few years, there has been renewed interest in C. diff diarrhea reflecting
a form of disease that is more frequent, more severe, and more refractory to standard
treatment. These observations are explained by the presence of a new strain of C. diff,
designated NAP-1, which produces more toxins A and B and is resistant.
Both C. difficile toxins A and B exhibit potent enterotoxic and cytotoxic effects that are
responsible for the clinical manifestations. The mechanism of action is by toxin binding on
intestinal receptors, leading to disruption of the cellular skeleton and intracellular junctions.
Protein synthesis and cell division are inhibited. Important inflammatory mediators attract
neutrophils and monocytes, increasing capillary permeability, tissue necrosis, hemorrhage,
and edema.
Clinical Presentation and Diagnosis. The clinical manifestations of C. diff may vary from
mild diarrhea to fulminant colitis. If a patient develops diarrhea several days to weeks (even
up to 8 weeks) after using antibiotics, evaluate for C. diff. Marked leukocytosis and systemic
symptoms are evident in severe cases.
Until a few years ago the diagnostic method of choice for C. difficile colitis was the enzymelinked immunosorbent assay (ELISA), based on toxin detection in the stool. While ELISA
is fast, relatively inexpensive, and has excellent specificity, its sensitivity is variable (ranging
75−85%). The newest preferred method of diagnosis is the nucleic acid amplification (LAMP,
loop-mediated isothermal amplification) assay, which may include the real-time polymerase
chain reaction (PCR) or loop-mediated isothermal amplification test, both of which detect
the toxin A and B genes responsible for the production of toxins. They have a sensitivity of
90−100% and a specificity of 94−100%. There is no benefit to testing multiple stool specimens or repeat testing following a positive test.
Treatment. Metronidazole is the drug of choice along with discontinuation of antibiotics (if
feasible) and supportive therapy. If the diagnosis is highly likely and the patient is seriously ill,
metronidazole may be given empirically before the test results. Oral vancomycin is reserved
for the following conditions:
• Failed therapy with metronidazole
• Organisms resistant to metronidazole
• Patient is allergic to or cannot tolerate metronidazole
• Patient is pregnant or a child age <10
• Patient is critically ill
If the symptoms resolve but there is a recurrence (~ 30% in some studies), then retreat with
metronidazole. Also, IV metronidazole can be used to treat C. difficile colitis if the patient is
unable to use oral medications. (This is not true of vancomycin. IV vancomycin will have no
effect in the bowel because it does not pass the bowel wall. Similarly, oral vancomycin will
have no systemic effect.)
94
A new drug, fidaxomicin, is not more effective than vancomycin or metronidazole for the first
episode. Fidaxomicin seems to decrease the number of episodes of recurrent C. difficile colitis.
Chapter 4
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Lactose Intolerance
Pathogenesis. Lactose intolerance is perhaps the single most common potential cause of diarrhea because of the enormously high prevalence of lactase deficiency. This is a disorder so common that the testing and treatment are generally empiric.
Clinical Presentation. The diarrhea produced is associated with gas and bloating, but never
has blood or leukocytes in it. Despite the malabsorption of lactose, weight loss does not occur.
Diagnosis and Treatment. A precise diagnosis can be established by finding an increased
stool osmolality and increased osmolar gap. The osmolar gap means that the difference
between the osmolality measure in the stool and the osmolality calculated from the sodium
and potassium levels is >50 mOsm/kg. In other words, the measured stool osmolality is greater than would be expected just by the level of sodium and potassium. The extra osmoles are
from lactose. Other causes of an increased stool osmolar gap are magnesium and polyethylene
glycol in the stool, also nutrient malabsorption → pancreatic insufficiency, celiac sprue, and
bacterial overgrowth.
The routine way to diagnose lactose intolerance is simply to remove milk, cheese, ice cream,
and all other dairy products (except yogurt) from the diet and observe for resolution of
symptoms, which should occur within 24 to 36 hours. (This is quite different from celiac disease, in which resolution of diarrheal symptoms make take weeks after stopping the ingestion
of gluten-containing foods.)
l Gastroenterology
If resolution of symptoms does occur within 24 to 36 hours, then dietary changes are the best
therapy. The patient can use lactase supplements.
Irritable Bowel Syndrome
Pathogenesis. Although it is often described at the same time as diarrheal illnesses, irritable
bowel syndrome (IBS) is predominantly a pain syndrome of unknown etiology. IBS is an idiopathic disorder in which there is increased frequency of the normal peristaltic and segmentation contractions of the bowel. Pain is often relieved by a bowel movement.
Clinical Presentation. Twenty percent of patients with IBS have constipation only. A large
number have diarrhea alone or diarrhea alternating with constipation. Everyone has pain.
No nocturnal symptoms. The majority are women with history of childhood abuse.
Diagnosis. There is no specific diagnostic test for IBS. The physician must first exclude lactose intolerance, inflammatory bowel disease, celiac disease, carcinoid, Giardia infection, and
anatomic defects of the bowel as the cause.
The diagnostic criteria, called Rome criteria, must occur for at least 3 months:
• Pain relieved by a bowel movement or by a change in bowel habit (e.g., when you
develop diarrhea, the pain goes away)
• Fewer symptoms at night
• Diarrhea alternating with constipation
No constitutional signs or symptoms, such as fever, weight loss, anorexia, or anemia.
Treatment. There is no clear definitive therapy for IBS. All patients should be placed on a highfiber diet in an attempt to increase the bulk of the stool. Those with diarrhea-predominant disease should receive antidiarrheal agents, such as loperamide or diphenoxylate.
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Antispasmodic agents are used on a trial-and-error basis until the most effective agent is
found. Examples of antispasmodics are hyoscyamine, dicyclomine, and the belladonna alkaloids. The presumptive mechanism of these agents is that they will relax the bowel wall musculature and diminish the pain.
Resistant cases may respond to tricyclic antidepressants. The presumptive mechanism is that
the tricyclics are anticholinergic and will relax the bowel. There is also a high frequency of
depression in many of these patients, and it is assumed that the tricyclics have an analgesic
effect with neuropathic pain.
A newer agent is tegaserod, which is used in constipation-predominant IBS. The major complication of therapy with tegaserod is diarrhea. Another newer agent is alosetron. Alosetron is
used in diarrhea-predominant IBS, and it slows motility. Both of these agents work by manipulating serotonin levels in the bowel.
Carcinoid Syndrome
Pathogenesis. Carcinoid syndrome describes tumors of the neuroendocrine system. They
are most often located in the appendix and the ileum. Bronchial carcinoids are rare but are
highly symptomatic because the serotonin produced from a bronchial carcinoid does not get
detoxified in the liver and is released directly into the circulation. With the exception of bronchial carcinoid, carcinoid syndrome by definition implies metastatic disease. Until there is an
enormous tumor burden, the liver is able to neutralize all of the serotonin released by the carcinoid in the bowel. This usually does not happen until the metabolic capacity of the liver has
been overwhelmed by metastatic disease.
Clinical Presentation. The presentation of carcinoid syndrome is with diarrhea, flushing, tachycardia, and hypotension. A rash may develop from niacin deficiency, which is a direct result of
the carcinoid. Serotonin and niacin are both produced from tryptophan. If there is an overproduction of serotonin, it produces a tryptophan deficiency, which leads to a deficiency of niacin.
Endocardial fibrosis also occurs because of a constant exposure of the right side of the heart to
the serotonin. This leads to tricuspid insufficiency and pulmonic stenosis.
Diagnosis. The diagnosis is confirmed with a urinary 5-hydroxyindolacetic acid level (5-HIAA).
Treatment. Therapy is generally based on controlling the diarrhea with octreotide, which is a
somatostatin analog. Very few carcinoids are sufficiently localized to be amenable to surgical
resection. If a tumor does happen to be localized, then it should be resected. This is most often
possible with bronchial carcinoid. Surgery is also used to relieve obstruction of the bowel.
MALABSORPTION SYNDROMES
Pathogenesis. The major causes of fat malabsorption are celiac disease and chronic pancreatitis,
although tropical sprue and Whipple disease are extremely rare but possible causes. What they
all have in common is the production of diarrhea characterized as greasy, oily, floating, and fatty,
with a particularly foul smell, as if fat were fermenting. This type of diarrhea with fat is referred
to as steatorrhea.
All malabsorption syndromes are characterized by weight loss because fat has the highest
caloric content of all the foods. In addition, there is malabsorption of the fat-soluble vitamins
A, D, E, and K. This can lead to hypocalcemia and easy bruising, as well as prolongation of the
prothrombin time.
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Iron malabsorption occurs if there is involvement of the duodenum where iron is normally
absorbed. Iron deficiency anemia is evident in all patients with celiac sprue. Macrocytic anemia results from folate being malabsorbed. Vitamin B12 malabsorption is from damage or
loss of the mucosal surface of the terminal ileum.
Clinical Presentation. All of the malabsorption syndromes present with chronic diarrhea. The
only unique feature of celiac disease is dermatitis herpetiformis. This is a vesicular skin rash on
the extensor surfaces of the body seen in approximately 10% of patients. Even without dermatitis
herpetiformis, celiac disease is the most likely etiology of fat malabsorption because it is the most
common.
l Gastroenterology
Patients with chronic pancreatitis will give a history of repeated episodes of pancreatitis from
alcohol or gallstones. Tropical sprue is suspected when there is a history of being in a tropical country. Whipple disease is by far the rarest. In addition to the usual presentation of a fat
malabsorption, Whipple disease is characterized by dementia (10%), arthralgias (80%), and
ophthalmoplegia.
Diagnosis. Celiac disease is first diagnosed by testing for the presence of antiendomysial
and antitransglutaminase antigliadin antibodies. The most accurate test is a small bowel
biopsy, which shows flattening of villi. Even if the antibody tests confirm the diagnosis of
celiac disease, the bowel biopsy should be done anyway to exclude small bowel lymphoma.
And because there is very little that is unique about tropical sprue, it is yet another reason to
always do a small bowel biopsy.
Just removing gluten (wheat, rye, and oats) from the diet is not a very accurate way of establishing the diagnosis because the circulating antibodies will continue to be present for weeks
after stopping the ingestion of gluten.
Chronic pancreatitis is diagnosed from the history of repeated episodes of pancreatitis and is
confirmed by finding calcification of the pancreas on x-ray and CT scan. The most accurate
test, although rarely done, is a secretin test, or finding a low trypsin level. Secretin normally
causes a voluminous release of bicarbonate and other pancreatic enzymes into the duodenum.
If you place a nasogastric tube into the duodenum and inject secretin into the blood, the pancreas will not release bicarbonate or enzymes into the duodenum in a patient with chronic
pancreatitis.
d-xylose testing was performed in the past to help distinguish between celiac disease and chron-
ic pancreatitis. d-xylose is a monosaccharide that requires no digestion to be absorbed. If there
is no absorption of d-xylose, it means there is a bowel-wall abnormality. d-xylose was absorbed
and excreted in chronic pancreatitis, but not in celiac disease, Whipple disease, or tropical sprue,
in which there is a bowel-wall abnormality. Antibody testing has largely replaced
d-xylose test-
ing. In addition, the presence of the deficiency of iron, folate, and carotene also point to a mucosal defect because they do not need pancreatic enzymes to be absorbed. Vitamin B12 is malabsorbed in pancreatic insufficiency and celiac disease. Pancreatic enzymes are necessary to absorb
B12. Vitamin K and calcium are malabsorbed because of fat malabsorption.
Clinical Pearl
Antibodies Seen in Celiac
Disease
• IgA endomysial antibody
• IgA tissue transglutaminase
antibody
• IgG tissue transglutaminase
antibody
• IgA deamidated gliadin
peptide
• IgG deamidated gliadin
peptide
Anti-tissue transglutaminase
antibody (IgA) is the most
sensitive and specific. In
patients with IgA deficiency,
IgA endomysial and
transglutaminase antibodies
are falsely normal.
Tropical sprue and Whipple’s disease are diagnosed by finding organisms on a bowel-wall
biopsy. The single most sensitive test for Whipple’s disease is a polymerase chain reaction
(PCR) of the bowel biopsy. A positive Tropheryma whippelii biopsy shows foamy macrophages
that are PAS positive.
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Treatment. Celiac disease is managed by adhering to a gluten-free diet (no wheat, oats, rye, or
barley). Dapsone is used when celiac patients have dermatitis herpetiformis. Chronic pancreatitis can be managed by orally replacing all the deficient enzymes. Amylase, lipase, and trypsin
can all be taken in a single combination pill. Tropical sprue is treated with trimethoprim/sulfamethoxazole or doxycycline for 6 months. Whipple’s disease is also treated with trimethoprim/
sulfamethoxazole or doxycycline, but it can also be treated with ceftriaxone for 1 year.
Although all malabsorption syndromes are associated with multiple deficiencies, note some
complications:
• Celiac disease is associated with GI lymphoma and adenocarcinoma; patients are at
risk for adenocarcinoma of the intestine.
• Celiac sprue is associated with lymphoma (enteropathy-associated T cell lymphoma)
(10-15% of cases); it is unclear whether therapy with gluten-free diet decreases incidence of lymphoma.
DIVERTICULAR DISEASE
Diverticulosis
Diverticulosis is so common in older populations in the Western world as to almost be considered simply a normal part of aging rather than a disease. Diverticulosis is presumably
caused by a lack of fiber in the diet to give bulk to stool. There is a subsequent rise in intracolonic pressure, leading to outpocketing of the colon. It is prevalent in 50% of persons age >50,
with even higher rates in older populations.
Clinical Presentation. Most of the time, these patients are asymptomatic. When they have
symptoms, it is of left lower quadrant abdominal pain that can be colicky in nature.
Diagnosis. Diverticulosis is diagnosed with colonoscopy. Endoscopy is superior to barium
studies, particularly when bleeding is present. Diverticula are more common on the left in
the sigmoid, but bleeding occurs more often from diverticula on the right because of thinner
mucosa and more fragile blood vessels. When bleeding occurs from diverticula, it is painless.
Treatment. Diverticulosis by itself is managed only with increasing fiber in the diet with products like Metamucil, dietary fiber in bran, or bulking agents, such as psyllium husks.
Diverticulitis
Diverticulitis is from an infection occurring in one of the diverticula. This occurs more frequently when there is a blockage of the diverticular entrance in the colon from nuts or corn.
Clinical Presentation. Diverticulitis is distinguished from uninfected diverticula by the presence of fever, tenderness, more intense pain, and an elevation of the white blood cell count in
the blood.
Diagnosis. Diverticulitis is confirmed by CT scanning. Barium studies and endoscopy are
relatively contraindicated in diverticulitis because there is a slightly higher risk of causing
perforation. There is no risk of perforation with CT scan.
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Treatment. Diverticulitis is treated with antibiotics such as ciprofloxacin and metronidazole.
The other choices are ampicillin/sulbactam, piperacillin/tazobactam, or the combination of
cefotetan or cefoxitin with gentamicin. Mild disease can be treated with oral antibiotics, such
as amoxicillin/clavulanic acid (Augmentin).
CONSTIPATION
A 72-year-old woman has a history of upper GI tract bleeding and iron-deficiency
anemia, for which she has recently been started on oral ferrous sulfate iron
replacement. She also has a history of diabetes with peripheral neuropathy, for
which she is on amitriptyline. She has untreated hypothyroidism, but is treated for
hypertension with nifedipine. Currently, she has constipation, and when the stool
does pass, it is very dark in color, almost black.
Pathogenesis. The most common cause of constipation is generally a lack of dietary fiber and
insufficient fluid intake. Calcium-channel blockers, oral ferrous sulfate, hypothyroidism, opiate analgesics, and medications with anticholinergic effects, such as the tricyclic antidepressants, all cause constipation. In the case of the patient described above, the most likely cause
of the constipation is the ferrous sulfate.
l Gastroenterology
Clinical Presentation. As written in the case, this patient’s stool is dark. This only occurs with
bleeding, bismuth subsalicylate ingestion, and iron replacement. However, GI bleeding gives
diarrhea and not constipation because blood acts as a cathartic. Blood causes diarrhea, and
iron tablets cause constipation.
Treatment. The general management is to stop medications that cause constipation, and
then to make sure the patient consumes 20–30 grams of fiber daily and is well hydrated.
Bulking agents, such as those used to manage diverticular diseases, are also helpful. Drug treatment of constipation includes milk of magnesia, cascara, bisacodyl, and docusate (Colace).
Enemas can be used for acute and serious constipation. Lactulose and polyethylene glycol
(GoLYTELY) can also be very effective.
COLON CANCER
Pathogenesis. The lifetime risk of colon cancer is >6%. Most cases occur sporadically, which
is to say there is no clearly identified etiology. Diets that are high in red meat and fat lead to
an increased risk for colon cancer, and smoking also increases the risk for colon cancer.
Clinical Presentation. Patients present with heme-positive, brown stool and chronic anemia
when the cancer is in the right side of the colon. Left-sided lesions and cancer of the sigmoid
colon are more often associated with symptoms of obstruction and with narrowing of stool
caliber. This is because the right side of the colon is wider, and the stool is more liquid in that
part of the bowel, making obstruction less likely on the right. Endocarditis by Streptococcus
bovis and Clostridium septicum is often associated with colon cancer. Any patient presenting
with endocarditis due to one of these organisms requires a GI work-up.
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