Professional Documents
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Gastroesophageal
junction
Nutrition Intervention Prior to treatment, patients with achalasia will need to have texture-modied
diets with increased caloric and protein density. Foods
that are extreme in temperature or very spicy should
also be avoided in order to prevent damage to esophageal mucosa. Smaller, more frequent feedings will be
tolerated best. After myotomy or dilatation, patients
should receive a texture-modied diet such as the
NDD-3 outlined in Table 14.11. A regular diet can be
resumed within 5 to 7 days of the procedure.
Pleura
Peritoneum
Peritoneal sac
Diaphragm
Hiatal Hernia
A - type 1 (sliding)
B - type 2 (rolling)
Hiatal hernia is a condition where the upper portion of the stomach protrudes through the esophageal
Reprinted from Price and Wilson: Pathophysiology: Clinical Concepts of Disease Processes, 6e
hiatus into the thoracic cavity. Most cases of hiatal
2006 Mosby with permission from Elsevier.
hernia are designated as type 1 (sliding) where both the
LES and some portion of the upper stomach protrude
considered together because they are controlled through the
through the esophageal hiatus or diaphragm into the chest (see
same neural pathways. Neural signals are sent to the vomiting
Figure 14.8). In type 2 (rolling hiatal hernia) the LES remains
center located in the medulla. As a result of these stimuli, the
below the diaphragm. Incidence of hiatal hernia increases with
steps of vomiting or emesis occur. In this sequence of events,
age. Any factor that increases intra-abdominal pressure, such
gastric contents are pushed upward by the constriction of the
as obesity or pregnancy, will also increase the risk of hiatal
respiratory muscles, the esophageal sphincter opens, the glottis
hernia.
closes (to prevent aspiration), and gastric contents are expelled
Symptoms of hiatal hernia are consistent with those of GERD.
through the mouth. Additionally, chemoreceptor zones in the
First-line interventions, both medically and nutritionally, are
medullary nucleus can also trigger the vomiting center. Drugs,
the same as those previously discussed for GERD. Some patoxins, metabolic conditions (such as renal failure or acid-base
tients do require surgical repair of the hernia. In this procedure,
imbalances), and motion aect chemoreceptor zones, which
which may be performed conventionally or laparoscopically,
can lead to nausea and emesis. Vomiting may also occur as a
the surgeon retracts the hernia and repairs the hole in the diaresult of stress or extreme emotions.
phragm. Fundoplication (previously described in the section on
Nausea and vomiting occur with many dierent medical condiGERD) can also be done at this time, if needed. The combinations. These may include infection, pain, pregnancy, syncope,
tion of surgical repair with fundoplication provides additional
headache, metabolic disorders, motion sickness, kidney failure,
support of the LES, which prevents the stomach from sliding
myocardial infarction, and a host of other possibilities. Thereback through the diaphragm.6, 31
fore, treatment of the underlying cause is the most important
step in treating nausea and vomiting. The patients history and
physical examination will assist in determining the cause of
nausea and vomiting. The etiology may be further claried after
Disease and clinical disorders that aect the stomach can cerassessment of the symptoms the patient experiences prior to
tainly inuence normal nutritional status. Some disorders, such
and after vomiting. For example, if vomiting occurs within a
as indigestion, are mild and temporary conditions that resolve
very short time after eating, it may be indicative of an obstruceasily. Others, such as peptic ulcer disease, are chronic and
tion.
Abdominal pain is symptomatic of an inammatory prorequire aggressive medical intervention.
cess. Simple regurgitation of food occurs when gastric contents
move easily from stomach to the mouth and is not a forceful
Indigestion
expulsion like that seen in vomiting.
Indigestion, or dyspepsia, is not considered to be a specic
After determining the etiology of nausea and vomiting, the
condition. Most people use the term indigestion to refer to
next step for treatment is use of medications or antiemeta wide range of symptoms that may include abdominal pain,
ics. Table 14.13 provides a summary of antiemetics used to
abdominal fullness, gas, bloating, belching, nausea, or even
treat nausea and vomiting. Medication action may decrease
gastroesophageal reux.
the sensitivity of the chemoreceptor trigger zones. In many
situations, such as in the use of chemotherapy, antiemetics
Nausea and Vomiting
are prescribed at the onset of treatment to prevent nausea.
Nausea is the unpleasant sensation that there is a need to
Controlling nausea from the very beginning of treatment
vomit; vomiting is the expulsion of gastric contents. Even
prevents anticipatory nausea and/or vomiting, which can octhough nausea does not always lead to vomiting, they are often
cur when there is a direct association between the nausea and
Chapter 14
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359
Table 14.13 Antiemetic Agents Used in the Treatment of Nausea and/or Vomiting
Generic and/or Trade Name
H1 antihistamines
Dimenhydrinate (Dramamine )
Diphenhydramine (Benadryl)
Hydroxyzine (Atarax)
Uses/Mechanism
Work by blocking histaminemay treat mild nausea such as motion
sickness; also provide benefit of mild relaxation. Not effective for severe
nausea and vomiting.
Benzamides
Metoclopramide (Reglan)
This medication blocks dopamine and therefore affects the vomiting center
in the brain. Side benefit of increasing gastric emptying.
Benzodiazepines
Diazepam (Valium)
Lorazepam (Ativan)
Butyrophenones
Droperidol (Inapsine)
This medication blocks dopamine and therefore affects the vomiting center
in the brain.
Phenothiazines
Prochlorperazine (Compazine)
This medication blocks dopamine and therefore affects the vomiting center
in the brain.
Corticosteroids
Dexamethasone
Methylprednisolone
Reduces the effect of prostaglandins and can also improve the effectiveness
of other antiemetics.
Dronabinol (Marinol)
Cannabinoids
NK1-receptor antagonists
Aprepitant (Emend )
Ondansetron (Zofran)
Tropisetron (Navoban)
Granisetron (Kytril)
Dolasetron (Anzemet)
Gastritis
Gastritis is inammation of the gastric mucosa. This condition is not a single disorder and may be a result of numerous
conditions. Under normal conditions, the gastric mucosa is
protected against injury. The production of mucus provides a
barrier that prevents damage to the cells, and their high turnover rate allows for ecient recovery from injury. Prostaglandins also assist in support of the mucosal defense by stimulating
mucus production, inhibiting acid production and release,
and regulating blood ow to the mucosal cells. Acute gastritis
is due to local irritation of the gastric mucosa. This irritation
can result from infections, such as with Helicobacter pylori
(H. pylori), food poisoning, alcohol ingestion, or medications
such as nonsteroidal anti-inammatory drugs (NSAIDs). By
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When there has been no vomiting for at least eight hours, start
oral intake slowly by adding one solid food at a time in very small
increments. Avoid food that high in fat or fiber as well as food that has a
strong odor or is gas producing. The use of ginger to treat nausea and
vomiting may help. Take medications after eating.
Yogurt, sherbet
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361
1982
Australian physicians Robin Warren and Barry Marshall rst
identify the link between Helicobacter pylorii (H. pylori) and
ulcers, concluding that the bacterium, not stress or diet,
causes ulcers. The medical community is slow to accept
their ndings.
1994
A National Institutes of Health Consensus Development
Conference concludes that there is a strong association
between H. pylorii and ulcer disease and recommends that
ulcer patients with H. pylorii infection be treated with antibiotics.
1995
Data show that about 75% of ulcer patients are still treated
primarily with antisecretory medications, and only 5% receive antibiotic therapy. Consumer research by the American Digestive Health Foundation nds that nearly 90% of
ulcer sufferers are unaware that H. pylorii causes ulcers. In
fact, nearly 90% of those with ulcers blame their ulcers on
stress or worry, and 60% point to diet.
1996
The Food and Drug Administration approves the rst antibiotic for treatment of ulcer disease.
1997
The Centers for Disease Control and Prevention (CDC), with
other government agencies, academic institutions, and industry, launches a national education campaign to inform health
care providers and consumers about the link between H. pylorii and ulcers. This campaign reinforces the news that ulcers
are a curable infection and the fact that health can be greatly
improved and money saved by disseminating information
about H. pylori. Medical researchers sequence the H. pylori
genome. This discovery can help scientists better understand
the bacterium and design more effective drugs to ght it.
2005
Nobel Prize for physiology or medicine awarded to Drs.
Barry J. Marshall and Robin Warren for proving that bacteria and not stress was the main cause of painful ulcers of
the stomach and intestine.
Sources:
Centers for Disease Control and Prevention [homepage on the Internet].
Atlanta: Centers for Disease Control and Prevention; 2001 Feb 2. History
of Ulcer Disease and Treatment. Available at http://www.cdc.gov/ulcer/
history.htm
Helicobacter pylori in Peptic Ulcer Disease, National Institutes of Health
Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease, Journal of the American Medical Association. 1994 July 6;272(1):
6569. Source: Centers for Disease Control and Prevention [homepage on
the Internet]. Atlanta: Centers for Disease Control and Prevention; 2001
Feb 2. History of Ulcer Disease and Treatment. Available at http://www.cdc
.gov/ulcer/history.htm
Marshall BJ, ed. Helicobacter pioneers: rsthand accounts from the
scientists who discovered helicobacters, 18921982. Victoria, Australia:
Blackwell; 2002.
Munnangi S., Sonnenberg A. Time trends of physician visits and treatment
patterns of peptic ulcer disease in the United States. Arch Intern Med. 1997
July 14;175:148994.
Parsonnet J Clinician-discoverersMarshall, Warren, and H. pylori. N Engl
J Med. 2005 Dec 8;353(23):242123.
(triple/quadruple therapy). The recommended therapy involves a 7- to 14-day course of two antibiotics with bismuth
and one of the proton pump inhibitors.71, 73, 77, 78 Eradication
rates associated with triple/quadruple therapy range from
86% to 98% if patients comply with triple/quadruple therapy
treatment regimens (see Table 14.15). However, frequently
occurring adverse eects such as nausea, vomiting, and
abdominal pain associated with these regimens signicantly
hinder patient compliance and most often the 7-day treatment is recommended.71, 73, 7779
Other treatment for PUD focuses on use of medications to
suppress acid secretion, which will ultimately promote healing of the ulceration (see Table 14.16). These medications,
as discussed in the section on treatment for GERD, include
antacids, proton pump inhibitors, histamine blocking agents,
prokinetic agents, and mucosal protectants. Because salicylates (aspirin) and NSAIDs are linked to increased gastric
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Metronidazole; tetracycline;
y
clarithromycin;
y
amoxicillin
Antacids
H2 blockers
Cytoprotective agents
Foods Recommended
Beverages
Eggs
Cereals
None
Potatoes/Rice/Pasta
Vegetables
All
Fruits
All
Fat
Dessert
Miscellaneous
Pepper
Chapter 14 Diseases of the Upper Gastrointestinal Tract
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363
Gastric Surgery
When peptic ulcer disease does not respond adequately to
medical treatment, or when the patient experiences a complication of PUD, surgery is often the next step. Complications
from PUD may include hemorrhage, perforation, or obstruction of the pyloric sphincter. These surgical procedures
are based on the patients current medical status and prior
surgical history. The same procedures are used for surgical resections required for other diagnoses such as gastric
malignancy.
Gastroduodenostomy (Billroth I); Gastrojejunostomy (Billroth II); Roux-en-Y Procedure Figure 14.9
illustrates these types of surgery. In the procedure gastroduodenostomy, or Billroth I, a partial gastrectomyy or pyloroplasty
is performed with a reconstruction that consists of an anastomosis of the proximal end of the duodenum to the distal end
of the stomach. A gastrojejunostomy, or Billroth II, is a partial
gastrectomy with a reconstruction that consists of an anastomosis of the proximal end of the jejunum to the distal end
Liver
Surgical
staples
Esophagus
Small stomach
pouch
Gallbladder
Duodenum
Stomach
(b)
Jejunum
Billroth II (after)
Large intestine
Liver
Sewn up
end of
duodenum
(c)
Sources: (a) John E. Pandolno, Brintha Krishnamoorthy, Thomas J. Lee. Gastrointestinal Complications of Obesity Surgery, Medscape General Medicine 6(2), 2004.
http://www.medscape.com/viewarticle/471952; (b, c) Diagrams reproduced with permission from CancerHelp UK, a free information service about cancer and cancer care
for people with cancer and their families. It is brought to you by Cancer Research UK. www.cancerhelp.org.uk
364
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