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NURSINGMANAGEMENT
OFGIT
PROBLEMS
GASTRIC ANDDUODENALDISORDERS
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GASTRITIS
Inflammation of the gastric mucosa. Often caused by dietary indiscretion or misuse
of
gastric irritating medications (aspirin, NSAIDs),
excessive alcohol intake, bile reflux and radiation
therapy.
Chronic gastritis and prolonged inflammation of
the stomach may be caused by either benign or
malignant ulcers of the stomach, or by the
bacteria Helicobacter pylori.
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GASTRITIS
The gastric mucous membrane becomes edematous and hyperemic and undergoes
superficial erosion.
Gastric mucosa secretes a scanty amount of
gastric juice, containing normal amount of
acid,
but very little mucus, and superficial erosions
may occur and can lead to hemorrhage.
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GASTRITIS
Clinical Manifestations: Abdominal discomfort
Headache, lassitude
Nausea, anorexia Vomiting
Singultus
Pyrosis
Belching
Sour taste in the mouth
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GASTRITIS
Diagnosis can be obtained by endoscopy,upper
GI radiographic studies, and histologic
examination of a tissue specimen obtained by
biopsy.
In addition to biopsy, other diagnosticmeasures
for detecting H. pylori include serologic testing
for antibodies against H. pylori antigen.
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GASTRITIS
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GASTRITIS
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GASTRITIS
Medical Management:Refrain from alcohol and food untilsymptoms subsideNon-irritating dietFluids may need to be administeredparenterallyCommon antacids to neutralize acidsEmetics and lavage are avoided because ofthe danger of perforation and damage to theesophagus.
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GASTRITIS
Medical Management:
Nasogastric intubation
Analgesic agents and sedatives
Fiberoptic endoscopy may be necessary
Emergency surgery to remove gangrenous or
perforated tissue
Diet modification
H. pylori may be treated with antibiotics and a
proton-pump inhibitor and possibly bismuth salts
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GASTRITIS
Nursing Management:
Assessment
Nursing Diagnoses
Planning and Goals
Nursing Interventions:
1. Reducing anxiety
2. Promoting optimal nutrition
3. Promoting fluid balance
4. Relieving pain
Promoting home and community-based care
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GASTRIC AND DUODENAL ULCERS
A peptic ulcer is an excavation that forms in the
mucosal wall of the stomach, in the pylorus, in
the duodenum, or in the esophagus.
Peptic ulcers are more likely to be in the
duodenum than in the stomach.
As a result, gastric ulcers tend to occur alone, but
they may occur in multiples.
Chronic gastric ulcers tend to occur in the lesser
curvature of the stomach, near the pylorus.
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GASTRIC AND DUODENAL ULCERS
Peptic ulcer disease occurs with the greatest
frequency in people between the ages of 40 and
60 years.
In the past, stress and anxiety were thought to be
causes of ulcers.
Familial tendency may be a significant
predisposing factor.
People with blood type O are more susceptible to
peptic ulcers than are those with blood type A, B,
or AB.
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GASTRIC AND DUODENAL ULCERS
Microbiologic etiology: Helicobacter pylori
Other predisposing factors: chronic NSAID
intake, alcohol ingestion, and excessive smoking.
Rarely ulcers are caused by excessive amounts of
the hormone gastrin, produced by tumors
(Zollinger-Ellison syndrome): severe peptic
ulcers, extreme gastric hyperacidity, and gastrinsecreting
benign or malignant tumors of the
pancreas.
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GASTRIC AND DUODENAL ULCERSDUODENAL ULCER GASTRIC ULCER
AGE 30 60 years Usually 50 and over
MALE:FEMALE RATIO 2-3:1 1:1
INCIDENCE 80% of peptic ulcers 15% of peptic ulcers
STOMACH ACID Hypersecretion Normal or hyposecretion
BODY WEIGHT Normal or weight gain Weight loss
EPIGASTRIC PAIN 2-3 hrs post-meal, early
morning awakenings,
relieved by food intake
- 1 hr post-meal, rarely
occurs at night; food intake
aggravates pain
VOMITING Uncommon Common (relieves pain)
HEMORRHAGE Less common, melena More common,hematemesis
PERFORATION More common Less common
MALIGNANCY Rare Occasionally
RISK FACTORS H. Pylori, alcohol,
smoking, cirrhosis, stress
H. pylori, gastritis, alcohol,
smoking, NSAIDs, stress
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GASTRIC AND DUODENAL ULCERS:
Pathophysiology
Peptic ulcers occur mainly in the gastroduodenal
mucosa because this tissue cannot withstand the
digestive action of gastric acid and pepsin.
Erosion is caused by increased concentration or
activity of acid pepsin, or by decreased resistance
of the mucosa.
The use of NSAIDs inhibits the secretion of
mucus that protects the mucosa.
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GASTRIC AND DUODENAL ULCERS:
Pathophysiology
Stress ulcer is the term given to the acute
mucosal ulceration of the duodenal or gastric area
that occurs after physiologically stressful events,
such as burns, shock, severe sepsis and multiple
organ traumas.
As the stressful condition continues, the ulcers
spread. When the patient recovers, the lesions
are reversed.
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GASTRIC AND DUODENAL ULCERS:
Pathophysiology
Cushings ulcers are common in patients with
trauma to the brain. They may occur in the
esophagus, stomach or duodenum and are usually
deeper and more penetrating than stress ulcers.
Curlings ulcers are frequently observed about 72
hours after extensive burns and involves the
antrum of the stomach or the duodenum.
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GASTRIC AND DUODENAL ULCERS:
Assessment
Endoscopy is the preferred diagnostic procedure
because it allows direct visualization of
inflammatory changes, ulcers and lesions.
Stools may be tested periodically until they are
negative for occult blood.
H. pylori infection may be determined by biopsy
and histology with culture, as well as a breath test
and serologic test for H. pylori antibodies.
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GASTRIC AND DUODENAL ULCERS:
Assessment
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GASTRIC AND DUODENAL ULCERS:
Assessment
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Medical Management:
Once the diagnosis is established, the patient is
informed that the problem can be controlled.
Recurrence may develop; however, peptic ulcers
treated with antibiotics to eradicate H. pylori
have a lower recurrence rate than those not
treated with antibiotics.
Methods include medications, lifestyle
modification, and surgical intervention.
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Medical Management: Pharmacologic
Therapy
Most commonly used therapy is a combination of
antibiotics, proton pump inhibitors, and bismuth
salts that suppresses or eradicates H. pylori.
Histamine-2 (H2) receptor antagonists and proton
pump inhibitors are used to treat NSAID-induced
and other ulcers not associated with H. pylori
ulcers.
Patient is advised to adhere to the medication
regimen to ensure complete healing of the ulcer.
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Medical Management: Stress
Reduction and Test
Reducing environmental stress requires physical
and psychological modifications on the patients
part as well as the aid and cooperation of family
members and significant others.
Identify situations that are stressful and
exhausting.
Biofeedback, hypnosis (?), or behavior
modification may be helpful.
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Medical Management:
Smoking Cessation
Studies have shown that smoking decreases the
secretion of bicarbonate from the pancreas into
the duodenum, resulting in increased acidity of
the duodenum.
Patient is strongly encouraged to stop smoking.
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Medical Management:
Dietary Modification
The intent is to avoid oversecretion of acid and
hypermotility of the GI tract.
Avoiding extremes of temperature and
overstimulation from consumption of meat
extracts, alcohol, coffee (including decaffeinated
coffee) and other caffeinated beverages, and diets
rich in milk and cream.
Neutralize acid by eating three regular meals a
day.
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Surgical Management
Surgery is usually recommended for patients with
intractable ulcers (those that fail to heal after 12
to 16 weeks of medical treatment), lifethreatening
hemorrhage, perforation, or
obstruction, and for those with ZES that do not
respond to medications.
Vagotomy, with or without pyloroplasty.
Billroth I (gastroduodenostomy) and Billroth II
(gastrojejunostomy) procedures.
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Follow-Up Care
Recurrence within a year may be prevented with
the prophylactic use of H2-receptor antagonists
given at a reduced dose. Not all patients require
maintenance therapy.
Likelihood of recurrence is reduced if th4e
patient avoids smoking, coffee and other
caffeinated beverages, alcohol, and ulcerogenic
medications.
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Follow-Up Care
Recurrence within a year may be prevented with
the prophylactic use of H2-receptor antagonists
given at a reduced dose. Not all patients require
maintenance therapy.
Likelihood of recurrence is reduced if th4e
patient avoids smoking, coffee and other
caffeinated beverages, alcohol, and ulcerogenic
medications.
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NURSINGMANAGEMENT
OFGIT
PROBLEMS
INTESTINALAND RECTALDISORDERS
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CONSTIPATION
Abnormal infrequency or irregularity of
defecation, abnormal hardening of the stools that
makes their passage difficult and sometimes
painful, a decrease in stool volume, or retention
of stool in the rectum for a prolonged period.
May be caused by certain medications, rectal or
anal disorders, obstruction, metabolic, neurologic
and neuromuscular conditions, endocrine
disorders, lead poisoning and connective tissue
disorders.
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CONSTIPATION: Pathophysiology
Poorly understood.
Interference with mucosal transport, myoelectric
activity, or processes of defecation.
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CONSTIPATION: Clinical Manifestations
Abdominal distention
Borborygmus
Pain and pressure
Decreased appetite
Headache, fatigue
Indigestion
Sensation of incomplete emptying
Passage of scybala
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CONSTIPATION: Assessment and
Diagnosis
Chronic constipation is usually considered
idiopathic, but secondary causes should be
eliminated.
Diagnosis is based on results of the patients
history, physical examination, possibly a barium
enema or sigmoidoscopy, and stool testing for
occult blood.
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CONSTIPATION: Assessment and
Diagnosis
Chronic constipation is usually considered
idiopathic, but secondary causes should be
eliminated.
Diagnosis is based on results of the patients
history, physical examination, possibly a barium
enema or sigmoidoscopy, and stool testing for
occult blood.
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CONSTIPATION: Complications
Hypertension
Fecal impaction
Hemorrhoids and fissures
Megacolon
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CONSTIPATION: Medical Management
Treatment is aimed at the underlying cause of
constipation and includes education, bowel habit
training, increased fiber and fluid intake, and
judicious use of laxatives.
Enemas and rectal suppositories are generally not
recommended for constipation and should be
reserved for the treatment of impaction or for
preparing the bowel for surgery or diagnostic
procedures.
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CONSTIPATION: Medical Management
Further studies are being carried out on
cholinergic agents (e.g., bethanechol),
cholinesterase inhibitors (e.g., neostigmine), and
prokinetic agents (e.g., metoclopramide) to
determine the role of these agents in treating
constipation.
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CONSTIPATION: Nursing Management
Elicit information about the onset and duration of
constipation, past and present elimination
patterns, the patients expectation of normal
bowel elimination, and lifestyle information
during health history review.
Past medical and surgical history, current
medications, and laxative and enema use are
important, as is information about the sensation
of rectal fullness or pressure, abdominal pain,
excessive straining at defecation and flatulence.
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CONSTIPATION: Nursing Management
Patient education and health promotion
Restoring and maintaining a regular pattern of
elimination
Ensuring adequate intake of fluids and high-fiber
foods
Teach methods to avoid constipation
Relieve anxiety about bowel elimination patterns
Avoid complications
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DIARRHEA
Increased frequency of bowel movements (more
than three per day), increased amount of stool
volume (more than 200 g per day), and altered
consistency (i.e., looseness) of stool.
Associated with urgency, perianal discomfort,
incontinence, or a combination of these factors.
Caused by increased intestinal secretions,
decreased mucosal absorption, or altered motility.
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DIARRHEA
Acute diarrhea is most often associated with
infection, and is usually self-limiting.
Chronic diarrhea persists for a longer period
(three weeks), and may return sporadically.
Diarrhea can be caused by certain medications,
tube feeding formulas, metabolic and endocrinedisorders, viral or bacterial infectious processes,
nutritional and malabsorptive disorders and anal
sphincter defects.
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DIARRHEA: Pathophysiology
Types of diarrhea: secretory, osmotic and mixed
diarrhea.
Secretory diarrhea is usually high-volume
diarrhea caused by increased production and
secretion of water and electrolytes by the
intestinal mucosa into the intestinal lumen. Osmotic diarrhea occurs when water is pulled
into the intestines by the osmotic pressure of
unabsorbed particles, slowing the reabsorption of
water.
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DIARRHEA: Pathophysiology
Mixed diarrhea is caused by increased peristalsis
(usually from IBD) and a combination of
increased secretion and decreased absorption in
the bowel.
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DIARRHEA: Clinical Manifestations
Increased frequency and fluid content of stools
Abdominal cramps and distention
Intestinal rumbling
Anorexia and thirst
Painful spasmodic contractions of the anus and
ineffectual straining (tenesmus) Watery stools are characteristic of small bowel
disease.
Loose, semisolid stools are associated more often
with disorders of the colon.
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DIARRHEA: Clinical Manifestations
Voluminous, greasy stools suggest intestinal
malabsorption.
Presence of mucus and pus suggests
inflammatory enteritis or colitis.
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DIARRHEA: Assessment and Diagnostic
Findings
Complete blood count
Chemical profile
Urinalysis
Routine stool examination
Stool examinations for parasitic or infectious
organisms, bacterial toxins, blood, fat andelectrolytes.
Barium enema may assist in identifying the
cause.
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DIARRHEA: Complications
Fluid and electrolyte imbalance (cardiac
dysrhythmias)
Renal failure
Multiorgan failure and death
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DIARRHEA: Medical Management
Primary management is directed at controlling
symptoms, preventing complications, and
eliminating or treating the underlying disease.
Certain medications may reduce the severity of
the diarrhea and treat the underlying disease.
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DIARRHEA: Nursing Management
Assess and monitor the characteristics and
pattern of diarrhea.
Encourage bed rest and intake of fluids and food
low in bulk until the acute attack subsides.
When food intake is tolerated, recommend a
bland diet of semisolid and solid food. Avoid caffeine, carbonated beverages and very
hot and very cold food.
Restrict milk products, fat, whole-grain products,
fresh fruits and vegetables for several days.
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DIARRHEA: Nursing Management
Administer antidiarrheal medications such as
diphenoxylate (Lomotil) and loperamide
(Imodium) as prescribed.
IV therapy for rapid rehydration especially for
the elderly and those with preexisting GI
conditions. Monitor serum electrolyte levels
Report immediately clinical evidence of
dysrhythmias or a change in the level of
consciousness.
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DIARRHEA: Nursing Management
The perianal area may be excoriated because
diarrheal stool contains digestive enzymes that
can irritate the skin. The patient should follow a
perianal skin care routine to decrease irritation
and excoriation.
Use skin sealants and moisture barriers asneeded.
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APPENDICITIS
The most common cause of acute abdomen in the
United States.
Males > females
Adolescents > adults
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APPENDICITIS: Assessment and
Diagnostic Findings
Diagnosis is based on results of a complete
physical examination and on laboratory and x-ray
findings.
Leukocytosis
Localized distention of the bowel or RLQ density
on abdominal x-ray films, sonographic ortomographic studies.
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APPENDICITIS: Complications
Perforation of the appendix
Peritonitis
Abscess
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APPENDICITIS: Medical Management
Surgery is indicated upon diagnosis.
Antibiotics and intravenous fluids are
administered until surgery is performed.
Analgesics may be administered in some patients
after the diagnosis is made.
Appendectomy is performed as soon as possibleto decrease the risk of perforation.
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APPENDICITIS: Nursing Management
Palliative Preoperative Care
Place patient in a comfortable position to relieve
abdominal pain and tension usually Fowlers
position.
See that the patient takes nothing by mouth to
decrease peristalsis and to allow stomach to emptypreparatory to surgery. Note time and nature of last
meal.
Place ice bag to right lower quadrant.
Do not administer cathartics.
Frequently evaluate vital signs.
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APPENDICITIS: Nursing Management
Operative
If diagnosis is established, a simple appendectomy is
performed.
Because relief is almost assured, patient usually
accepts surgery very willingly, which afford a smooth
recovery. Anesthetic may be general or spinal.
Incision may be McBurney, muscle splitting or gridiron,
or right rectus.
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APPENDICITIS: Nursing Management
Postoperative Care
Following recovery from anesthetic, Fowlers position
is maintained, analgesic is given every 3 or 4 hours as
needed, and fluids and food are given as tolerated.
Stitches are removed between 5th and 7th day (usually
in the physicians office).
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APPENDICITIS: Nursing Management
Goals: relieve pain, prevent fluid volume deficit,
reduce anxiety, eliminate infection, maintain skin
integrity, and attain optimal nutrition
Prepare patient for surgery
NGT insertion
Avoid enema Post-operative care
Instruction for wound care prior to discharge
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APPENDICITIS: Nursing Management
Goals: relieve pain, prevent fluid volume deficit,
reduce anxiety, eliminate infection, maintain skin
integrity, and attain optimal nutrition
Prepare patient for surgery
NGT insertion
Avoid enema Post-operative care
Instruction for wound care prior to discharge
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INFLAMMATORY BOWEL DISEASE
Refers to two chronic inflammatory GI disorders:
regional enteritis (i.e., Crohns disease or
granulomatous colitis) and ulcerative colitis.
The cause is still unknown.
Researchers think it is triggered by
environmental agents such as pesticides, foodadditives, tobacco, and radiation.
NSAIDs have been found to exacerbate IBD.
Allergies and immune disorders have also been
suggested as causes.
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INFLAMMATORY BOWEL DISEASE
CROHNS DISEASE ULCERATIVE COLITIS
COURSE Prolonged, variable Exacerbations, remissions
EARLY PATHOLOGY Transmural thickening Mucosal ulceration
LATE PATHOLOGY Deep, penetrating
granulomas
Mucosal minute ulcerations
LOCATION Ileum, right colon (usually) Rectum, left colon
BLEEDING Usually not, but may occur Common severe
PERIANAL
INVOLVEMENT
Common Rare mild
FISTULAS Common RareRECTAL
INVOLVEMENT
About 20% Almost 100%
DIARRHEA Less severe Severe
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INFLAMMATORY BOWEL DISEASE
CROHNS DISEASE ULCERATIVE COLITIS
RADIOGRAPHY Regional, discontinuous
lesions
Narrowing of colon
Thickening of bowel wall
Mucosal edemaStenosis, fistulas
Diffuse involvement
No narrowing of colon
No mucosal edema
Stenosis rare
Shortening of colonAbnormal inflamed mucosa
SIGMOIDOSCOPY May be unremarkable
unless accompanied by
perianal fistulas
Abnormal inflammed
mucosa
COLONOSCOPY Distinct ulcerations
separated by relatively
normal mucosa in the
right colon
Friable mucosa with
pseudopolypsor ulcers in
the left colon
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INFLAMMATORY BOWEL DISEASE
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COLORECTAL CANCER
The colorectal area is the third most common site
of new cancer cases and deaths.
Incidence increases with age and is higher for
people with a family history of colon cancer and
those with IBD or polyps.
Risk factors:
Increasing age
Past and family history of colon cancer, polyps, IBD
High-fat, high-protein, low-fiber diet
Genital or breast cancer (in women)
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COLORECTAL CANCER:
Pathophysiology
Predominantly (95%) adenocarcinoma.
Usually starts as a benign polyp but may become
malignant, invade and destroy normal tissues,
and extend into surrounding structures.
Cancer cells may break away from the primary
tumor and spread to other parts of the body (most
often the liver).
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COLORECTAL CANCER:
Clinical Manifestations
Determined by the location of the cancer, the
stage of the disease, and the function of the
intestinal segment in which it is located.
Change in bowel habits
Passage of blood in the stools
Unexplained anemia, anorexia, weight loss and
fatigue
Dull abdominal pain and melena (right colon)
Abdominal pain, cramping, narrowing stools,
constipation and distention (left colon)
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COLORECTAL CANCER:
Clinical Manifestations
Tenesmus, rectal pain, feeling of incomplete
evacuation after a bowel movement, alternating
diarrhea and constipation and bloody stool (rectal
lesions)
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COLORECTAL CANCER:
Assessment and Diagnosis
Abdominal and rectal examination
Fecal occult blood testing
Barium enema
Proctosigmoidoscopy and colonoscopy with
biopsy or cytology smears
CEA studies for prognostication
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COLORECTAL CANCER:
Assessment and Diagnosis
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COLORECTAL CANCER:
Assessment and Diagnosis
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COLORECTAL CANCER:
Medical Management
Depends on the stage of the disease
Surgery to remove the tumor
Supportive therapy
Adjuvant therapy
Chemotherapy
Radiation therapy
Immunotherapy
Multimodality therapy
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ANORECTAL DISEASES:
Hemorrhoids
Dilated portions of veins in the anal canal
Internal hemorrhoids vs external hemorrhoids
Cause itching and pain and the most common
cause of bright red bleeding with defecation
Symptoms and discomfort can be relieved by
good personal hygiene and by avoiding excessive
straining during defecation.
High residue diet that contains fruit and bran
along with an increased fluid intake may be all
the treatment that is necessary.
A O C AL IS AS S
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ANORECTAL DISEASES:
Hemorrhoids
Warm compresses, sitz baths, analgesic
ointments and suppositories, astringents, and bed
rest allow the engorgement to subside.
Nonsurgical treatments: infrared
photocoagulation, bipolar diathermy and laser
therapy, sclerosing solutions
Surgical treatment: rubber band ligation,
cryosurgery, hemorrhoidectomy
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NURSINGMANAGEMENT
OFGIT
PROBLEMS
HEPATIC,BILLIARY
SYSTEM ANDPANCREAS
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HEPATITIS
Hepatitis is an inflammation of the liver caused
by a variety of factors; most infectious etiologies
are viral in nature.
Significance:
From a community health perspective, one is
concerned with ease of disease transmission and
morbidity.
From a socioeconomic viewpoint, one is concerned
with prolonged loss of time from school and
employment.
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HEPATITIS
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HEPATITISHAV HBV HCV HDV HEV
Incubation(days) 15-45,mean 30 30-180, mean60-90 15-160,mean 50 30-180,mean 60-90 14-60,mean 40
Onset Acute Insidious or
acute
Insidious Insidious or
acute
Acute
Age
preference
Children,
young
adults
Young
adults,
babies,toddlers
Any age,
but more
commonin adults
Any age
(similar to
HBV)
Young
adults
(20-40years)
Transmission Fecal-
oral
Percutaneous
Perinatal
Sexual
Similar to
HBV
Similar to
HBV
Fecal-oral
Severity Mild Occasionallysevere Moderate Occasionallysevere Mild
Fulminant 0.1% 0.1-1% 0.1% 5-20% 1-2%
Progression to
chronicity
None Occasional (1-
10%, 90%
of neonates)
Common Common None
HEPATITIS
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HEPATITIS
HAV HBV HCV HDV HEV
Carrier None 0.1-30% 0.5-1% Variable None
Cancer None + (neonatal
infection)
+ + or - None
Prognosis Excellent Worse with
age, debility
Moderate Acute, Good
Chronic,
poor
Good
Prophylaxis IG
vaccine
HBIG
Recombinant
vaccine
None HBV vaccine
(none for
HBV
carriers)
Unknown
Therapy None Interferon
40% effective
Interferon
50%
response;
sustained
response
< 15%
Unknown None
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HEPATITIS A
Epidemiology
RNA virus of the enterovirus family
Mode of transmission:
Feca-oral route; respiratory route possible
Poor sanitation; person-to-person (epidemic type)
Contaminated food, milk, polluted water, or shell fish
Blood transfusion rarely
Incubation: 3 to 7 weeks; average 4 weeks
Occurrence:
Worldwide
Usually children and young adults
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HEPATITIS B
Epidemiology
Double-shelled virus containing DNA
Causative agent is composed of:
Antigenic material in an outer coat hepatitis B surface
antigen (HBsAg)
Antigenic material in an inner coat hepatitis B core antigen
(HBcAg)
An independent protein circulating in the blood (HBeAg)
Antibody:
Anti-HBs produced early after infection
Anti-HBc noted later in convalescence
Anti-Hbe noted later in convalescence
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HEPATITIS B
Epidemiology
Double-shelled virus containing DNA
Causative agent is composed of:
Antigenic material in an outer coat hepatitis B surface
antigen (HBsAg)
Antigenic material in an inner coat hepatitis B core antigen
(HBcAg)
An independent protein circulating in the blood (HBeAg)
Antibody:
Anti-HBs produced early after infection
Anti-HBc noted later in convalescence
Anti-Hbe noted later in convalescence
HEPATITIS B
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HEPATITIS BCOMMONLY ENCOUNTERED SEROLOGIC PATTERNS OF HEPATITIS B INFECTION
HBsAg Anti-HBs Anti-HBc HB-eAG Anti-HBe Interpretation
+ - IgM + - Acute HBV infection, high
infectivity
+ - IgG + - Chronic HBV infection, high
infectivity
+ - IgG - + Late-acute or chronic HBVinfection, low infectivity
+ + + + or - + or - 1. HBsAg of one
subtype and
heterotypic anti-
HBs (common)
2. Process ofseroconversion
- - IgM + or - + or - 1. Acute HBV
infection
2. Anti-HBc window
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HEPATITIS B
Epidemiology
Mode of transmission:
Oral-oral via saliva
Parenterally or via intimate contact with carriers
Male homosexuals
Blood, saliva, semen, vaginal secretions
Incubation: 2 to 5 months
Occurrence: affects all ages but mostly young adults
worldwide
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HEPATITIS B
Assessment
Resembles Hepatitis A clinically.
Symptoms insidious and variable.
Arthralgias and rashes may be observed; fever and
respiratory symptoms are rare.
Jaundice may or may not be present.
Anorexia, abdominal pain, generalized ailing, malaise
may be noted.
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HEPATITIS B
Nursing Management
Provide adequate fluids, nutrition and bed rest.
Administer alkalis, belladonna and antiemetics if
these agents are required to control dyspepsia and
malaise.
A newly available gamma globulin with a high titer of
anti HBs seems to reduce severity of hepatitis
following needle-stick exposure or contact.
Recognize that recovery and convalescence are slow
and prolonged, sometimes taking 3 to 4 months;
provide psychosocial stimulation.
Hepatitis vaccination
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HEPATITIS CIRRHOSIS
Cirrhosis of the liver is a chronic disease in
which there has been diffuse destruction of
parenchymal cells followed by degeneration and
increase in connective tissue.
Classification:
Laennecs cirrhosis alcoholic
Postnecrotic
Biliary
Posthepatitic
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HEPATITIS CIRRHOSIS
Nursing Management
Instruct and prepare patient for the very many
laboratory studies.
Evaluate nutritional status and needs.
Monitor intake and output accurately.
Adjust nutritional offerings if the patient has ascites
and edema.
Assist the patient in overcoming anorexia, weight loss
and fatigue.
Observe skin and control pruritus.
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HEPATITIS CIRRHOSIS
Nursing Management
Recognize the effect of esthetic factors.
Eliminate alcohol but encourage high caloric intake.
Give supplementary vitamins.
Be cognizant of signs of hematemesis and melena.
Anticipate manifestations of hemorrhage.
Recognize signs of increasing stupor.
Health education
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HEPATITIS ENCEPALOPATHY
Nursing Management
Recognize the effect of esthetic factors.
Eliminate alcohol but encourage high caloric intake.
Give supplementary vitamins.
Be cognizant of signs of hematemesis and melena.
Anticipate manifestations of hemorrhage.
Recognize signs of increasing stupor.
Health education
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HEPATITIS ENCEPALOPATHY
Precipitating Factors
Progressive hepatocellular disease
Increased sources of ammonia in the blood
Infections, paracentesis, acute alcoholism,
hypotension, shock, general anesthesia, minor
surgery, hypokalemia, alkalosis, administration of
sedatives or narcotics.
Portocaval shunts
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HEPATITIS ENCEPALOPATHY
Nursing Management
Evaluate the patients vital functions.
Arrest gastrointestinal bleeding and reduce
intraintestinal nitrogen.
Reduce and possibly eliminate all sedatives and
analgesics.Administer only those specifically
prescribed.
Prevent complications.
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GALLBLADDER DISEASE
Types
Cholecystitis (inflammation of the gall bladder)
Cholelithiasis (stones in the gall bladder)
Choledocholithiasis (stones in the common bile duct)
Assessment and Clinical Manifestations
History of episodic and usually colicky epigastric or
RUQ pain associated with nausea and vomiting.
Jaundice (?)
Murphys sign
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GALLBLADDER DISEASE
Treatment
Surgery is advised if gallstones are present.
In older patients, the risk of surgery must be evaluated
in relation to other disease conditions present.
Chenodeoxycholic acid can decrease the size of an
existing stone and prevent new stones from forming.
For acute cholecystitis, provide hospitalization, bed
rest, withholding of oral fluids, and insertion of
nasogastric tube with suction.
Administer IV fluids to correct electrolyte imbalances,
maintain adequate UO and provide nutritional needs.
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GALLBLADDER DISEASE
Treatment
Administer medication for pain and infection control.
Prepare for laboratory studies.
Record vital signs every 4 hours and prepare for
surgery.
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ACUTE PANCREATITIS
Acute pancreatitis is an inflammation of the
pancreas brought about by the digestion of this
organ by enzymes.
Etiology
Unknown
Associated with excessive intake of alcohol
Associated with blockage of the ampulla of Vater by
gallstones
Associated with spasm and edema of the ampulla of
Vater following duodenitis or after treatment with
opiates.
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ACUTE PANCREATITIS
Etiology
May occur as a complication of mumps or bacterial
disease.
Some congenital hyperlipidemias appear to be related
to acute pancreatitis.
Clinical Manifestations
Abdominal and back pain
Nausea, vomiting and fever
Tenderness across upper abdomen often minimal
Elevated lipase and amylase
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ACUTE PANCREATITIS
Nursing Management
Relieve discomfort and pain to control restlessness
Give meperidine (Demerol)
Encourage patient to assume position of comfort
Decrease pancreatic secretions by reducing
stimulation
NPO
Anticholinergic medications
NGT insertion
Maintain comfort of the intubated patient
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ACUTE PANCREATITIS
Nursing Management
Monitor patient for signs of respiratory failure.
Provide medications to correct deficiencies and
prevent complications
Parenteral fluids, electrolytes, blood and plasma; accurate I
and O.
Antimicrobials
Control of hyperglycemia
Support cardiopulmonary system
Surgical intervention (controversial)
Health education and discharge planning