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GIT DISORDERS
BY
SAMAR FALTAS
UNDERSUPERVISION OF
PROF.DR/ MAGD ABD EL-AZIZ
Outlines
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Introduction
The Gastrointestinal Tract
How to Diagnose Gastrointestinal Problems
Common GIT disorders:
Hernia
Oral cancer
Peritonitis
GERD
Intestinal obstruction
Hital hernia
Hemorrhoids
Gastritis
Hepatitis
Peptic ulcer disease
Liver cirrhosis
Upper GIT bleed
Assessment & management of gastrointestinal disorders
Objectives
At the end of this presentation the audience will be
able to:
• Identify how to Diagnose Gastrointestinal Problems
• Determine Common GIT disorders such as; oral
cancer, GERD, peptic ulcer,…….
• Apply Assessment & management
of
gastrointestinal disorders
Introduction
• It is estimated that some form of digestive
disorder affects more than 100 million people
in America. That is more than half of the U.S.
population. (WHO ,2009)
• For some people, digestive disorders are a
source of irritation and discomfort that may
cause them to drastically limit their lifestyles
and to frequently miss work. For others, the
disorders may be extremely crippling and even
fatal.
The Gastrointestinal Tract
• The gastrointestinal tract (GIT) is a long muscular
tube that functions as the food processor for the
human body.
• The digestive system includes
the following organs:
 Upper GIT (mouth, esophagus
stomach and duodenum) .
 Accessory digestive organs
(Gallbladder, liver, and pancreatic) .
 Lower GIT.
How to Diagnose Gastrointestinal
Problems
• Physical examination
• Endoscopy: by use a small camera to look at the
lining of stomach, esophagus and initial part of small
intestine. The camera inserts into mouth and
progresses down the gastrointestinal tract.
• Fluoroscopy : to examine the moving body structures.
This procedure consists of an x-ray which shows the
body area being examined and projects images onto a
monitor so the physician can observe the movements
of the stomach, duodenum and esophagus.
• (ERC) Endoscopic retrograde cholangiopancreato
graph :can examine any problems with gallbladder,
liver and pancreas. patient swallow the scope, and the
doctor directs a camera to the spot where the ducts to
the pancreas open into the duodenum. Then injects
dye into the ducts to visualize the area and determine
a course of treatment.
• liver biopsy: If patient have any issues with liver take
biopsy to examine tissue and assess if there is any
disease. This usually occurs after blood tests indicate
a potential problem with liver.
• Fecal analysis : Fecal content is an indicator of the
absorptive capacity of the gut
D-Xylose absorption test : D-Xylose, a
monosaccharide, is absorbed in
the
small intestine and is used to assess
malabsorption
 The client receives nothing by mouth
(NPO) for 10 to 12 hours before the test.
 A blood sample and first-voided morning
urine specimen are collected.
 After oral administration of a known
quantity of D-Xylose mixed in water, blood
and urine levels of D-Xylose are measured
•
• Bernstein test (Esophageal acidity, esophageal
manometry,
acid perfusion): is measured to
diagnosis problems of the lower esophageal sphincter
and chronic reflux esophagitis.
 A catheter with a pH electrode is inserted
into the
esophagus through the mouth
• Barium swallow: To diagnosis esophageal varices,
inflammation, ulcerations, hiatal hernia, foreign
bodies, polyps, diverticula, and tumors of the
esophagus, stomach, and duodenal bulb
 Client will drink 16-20 ounces of a chalky
liquid (barium sulfate before the exam and
observing the movement of a contrast
medium with a fluoroscope
• Magnetic resonance imaging (MRI): To
identify source of gastric bleeding
• Gastric analysis: To evaluate gastric secretions
and detect an
increase or decrease of free
hydrochloric acid ( fasting:1.0-5.0 mEq/per
hour
 To conduct the gastric analysis, a
nasogastric
tube is inserted into the
stomach and specimens are aspirated to
evaluate gastric acidity
Common GIT disorders
Oral cancer
Hernia
GERD
Peritonitis
Hital hernia
Intestinal obstruction
Gastritis
Hemorrhoids
Peptic ulcer disease
Hepatitis
Upper GIT bleed
Liver cirrhosis
Oral cancer
• Uncommon (5% of all cancers) but
has
high
rate
of
morbidity,
mortality.
• Highest among males over age 40.
• Risk factors include smoking and
using
oral
tobacco,
drinking
alcohol,
marijuana
use,
occupational exposure to chemicals
Pathophysiology
• Squamous cell carcinomas
• Begin as painless oral ulceration
or lesion with irregular, illdefined borders
• Lesions start in mucosa and may
advance to involve tongue,
oropharynx, mandible, maxilla
• Non-healing lesions should be
evaluated for malignancy after
one week of treatment
• Diagnosed by biopsy, CT, MRI
• Based on age, tumor stage, general health
and client’s preference, treatment may
include surgery, chemotherapy, and/or
radiation therapy
• Advanced carcinomas may necessitate
radical neck dissection with temporary or
permanent tracheostomy.
Gastroesophageal Reflux
Disease (GERD)
• GERD is the backward flow of gastric
content into the esophagus
• common, affecting 15 – 20% of adults
• 10% persons experience daily heartburn
and indigestion
• symptoms may mimic other illnesses
including heart problems because of
location near other organs
•
o
o
o
o
Gastroesophageal reflux results from
transient relaxation or incompetence of
lower esophageal sphincter, or increased
pressure within stomach which may
result from:
Increased gastric volume (post meals)
Position pushing gastric contents close to
gastroes-ophageal juncture (such as
bending or lying down)
Obesity or tight clothing
Hiatal hernia
Manifestations
• Heartburn after meals, while bending
over, or recumbent
• May have regurgitation of sour
materials in mouth, pain with
swallowing
• Atypical chest pain
• Sore throat with hoarseness voice
• Bronchospasm and laryngospasm
Diagnostic Tests
• Barium swallow (evaluation of
esophagus,
stomach,
small
intestine)
• Upper
endoscopy:
direct
visualization; biopsies may be done
• 24-hour ambulatory pH monitoring
• Esophageal
manometry,
which
measure pressures of esophageal
sphincter and peristalsis
• Esophageal motility studies
Medications
• Antacids for mild to moderate symptoms,
e.g. Maalox, Mylanta, Gaviscon
• H2-receptor blockers:
decrease acid
production; e.g. cimetidine, ranitidine,
famotidine, nizatidine
• Proton-pump inhibitors: reduce gastric
secretions, promote healing of esophageal
erosion
and
relieve
symptoms,
e.g.
omeprazole (prilosec); lansoprazole (Prevacid)
initially for 8 weeks; or 3 to 6 months
• Promotility agent: enhances esophageal
clearance and gastric emptying, e.g.
metoclopramide (reglan)
Dietary and Lifestyle Management
• Elimination of acid foods (tomatoes, spicy,
citrus foods, coffee)
• Avoiding food which relax esophageal sphincter
or delay gastric emptying (fatty foods,
chocolate, peppermint, alcohol)
• Maintain ideal body weight
• Eat small meals and stay upright 2 hours post
eating; no eating 3 hours prior to going to bed
• Elevate head of bed on 30 degree to decrease
reflux
• No smoking
• Avoiding bending and wear loose fitting
clothing
Hiatal Hernia
• Part of stomach protrudes through the
esophageal (hiatus of the diaphragm into
thoracic cavity).
• Sliding hiatal hernia :gastro esophageal junction
and funds of stomach slide through the
esophageal hiatus
• Para esophageal hiatal hernia: the gastro
esophageal junction is in normal place but part
of stomach herniated through esophageal hiatus
• Predisposing factors include:
–
–
–
–
–
Increased intra-abdominal pressure
Increased age
Trauma
Congenital weakness
Forced recumbent position
Manifestations: Similar to GERD
Diagnostic Tests
• Barium swallow
• Upper endoscopy
Treatment
• surgery; usually Nissen fundoplication by thoracic
or abdominal approach
– Anchoring the lower esophageal sphincter by wrapping a
portion of the stomach around it to anchor it in place
Nissen fundoplication
Gastritis
• Inflammation of stomach lining from irritation
of gastric mucosa
Types
• Acute Gastritis: Disruption of mucosal barrier
allowing hydrochloric acid and pepsin to have
contact with gastric tissue: leads to irritation,
inflammation, superficial erosions
• Progressive disorder beginning with superficial
inflammation and leads to atrophy of gastric
tissues
Causes
• Irritants include aspirin and other NSAIDS,
corticosteroids, alcohol, caffeine
• Ingestion of corrosive substances: alkali or acid
• Effects
from
radiation
therapy,
certain
chemotherapeutic agents
Manifestations
• Mild: anorexia, mild epigastric discomfort,
belching
• More severe: abdominal pain, nausea, vomiting,
hematemesis, melena
• Erosive: not associated with pain; bleeding
occurs 2 or more days post stress event
• If perforation occurs, signs of peritonitis
Diagnostic Tests
• Gastric analysis: assess hydrochloric
acid secretion
• Hemoglobin, hematocrit, red blood cell
indices: anemia including pernicious or
iron deficiency
• Serum vitamin B12 levels: determine
pernicious anemia
• Upper endoscopy: visualize mucosa,
identify areas of bleeding, obtain
biopsies; may treat areas of bleeding
with electro or laser coagulation or
sclerosing agent
Peptic Ulcer
• Break in mucous lining of GI tract
comes into contact with gastric juice
often involves the deeper structures of
the upper gastrointestinal tract e.g.,
esophagus, stomach, duodenum, or
jejunum
• Common in smokers, users of NSAIDS;
familial pattern, alcohol, cigarettes
Pathophysiology
• Ulcers or breaks in mucosa of GI tract occur
with
 H. pylori infection (spread by oral to oral,
fecal-oral routes) damages gastric epithelial
cells reducing effectiveness of gastric mucus
 Use of NSAIDS: interrupts prostaglandin
synthesis which maintains mucous barrier of
gastric mucosa
 Chronic with spontaneous remissions and
exacerbations associated with trauma,
infection, physical or psychological stress
Acid secretion
• Gastric acid secreted by the parietal cell in the fundus
at the stomach in response to:
 Gastrin (secreted by cells in the pyloric region )
 Acetylcholine (cholinergic action of the vagus nerve)
 Histamine (found in cells throughout the gastric
mucosa
• Diagnosis
– Endoscopy with cultures
• Looking for H. Pylori
– Upper GI barium contrast studies
– EGD-esophagogastroduodeno scopy
– Serum and stool studies
Stomach structure
Sites of ulcer
Peptic ulcer
Manifestation
 Pain is classic symptom:
gnawing,
burning, aching hunger like in epigastric
region possibly radiating to back; occurs
when stomach is empty and relieved by
food (pain: food: relief pattern)
 Symptoms less clear in older adult; may
have
poorly
localized
discomfort,
dysphagia, weight loss
 Complication:
GI
hemorrhage
or
perforation of stomach or duodenum
Treatment
– Rest and stress reduction
– Nutritional management
– Pharmacological management
 Histamine blockers (Tagamet, Zantac, Axid)
• Blocks gastric acid secretion
 Carafate
• Forms protective layer over the site
 Mucosal barrier enhancers (colloidal bismuth,
prostoglandins)
• Protect mucosa from injury
 Antibiotics (Amoxicillin):Treat H. Pylori
infection
• NG suction
• Surgical intervention
1. Minimally invasive gastrectomy
• Partial gastric removal with laproscopic surgery
2. Bilroth I and II
• Removal of portions of the stomach
3. Vagotomy
• Cutting of the vagus nerve to decrease acid secretion
4.Pyloroplasty
• Widens the pyloric sphincter
5.Gastrectomy (roux-en-y)
Remove antrum
Bilroth I
Bilroth II
Bilroth I & Bilroth II
Vagotomy
Pyloroplasty
Gastrectomy
Complications
• Hemorrhage:
hematemesis,
melena,
hematochezia (blood in stool)
• weakness, fatigue, dizziness, orthostatic
hypotension and anemia
• Gastric
outlet
(pyloric
sphincter)
obstruction: edema surrounding ulcer
blocks GI tract from muscle spasm or scar
tissue leads to feelings of epigastric fullness,
nausea, worsened ulcer symptoms
• Perforation: ulcer erodes through mucosal
wall and gastric or duodenal contents enter
peritoneum leading to peritonitis; chemical
at first (inflammatory) and then bacterial
in 6 to 12 hours with the following:
1.severe upper abdominal pain radiating
throughout abdomen and possibly to shoulder
2.Abdomen becomes rigid, board like with
absent bowel sounds; symptoms of shock
3.Older adults may present with mental
confusion and non-specific symptoms
Upper GI Bleed
• Mortality approx 10%
• Predisposing factors include: drugs,
esophageal
varacies,
esophagitis,
peptic ulcer diseases, gastritis and
carcinoma
• Diagnosis
– History
– Blood, stool, vomitus studies
– Endoscopy
• Signs and Symptoms
Coffee ground vomitus
Black, tarry stools
Melena
Decreased B/P
Vertigo
Drop in Hct, Hgb
Confusion
syncope
• Treatments
Volume replacement
• Crystalloids- normal saline
• Blood transfusions
NG lavage
Endoscopic treatment of bleeding ulcer
Sclerotheraphy-injecting bleeding ulcer
with necrotizing agent to stop bleeding
Sengstaken-Blakemore tube
• Used with bleeding esophageal varacies
Sengstaken-Blakemore tube
•
A tube used for the tamponade of bleeding
esophageal varacies. It has three separate small
tubes;
1. One leads to a balloon inflated in the stomach, to
keep the instrument in place and compress the
vessels around the cardia;
2. The second leads to a long narrow balloon that
exerts pressure against the wall of the esophagus;
3. The third is attached to a suction apparatus for
aspirating the contents of the stomach.
Sengstaken-Blakemore tube
Hernia
• It is an abnormal protrusion of the
intestine or other abdominal organ
through a weakness or defect in the
musculature into another cavity.
• Hernia is the protrusion of an organ
or tissue out of the body cavity in
which it normally lies.
• Caused by a congenital or acquired
abdominal muscle weakness as
Obesity, Pregnancy, or Occupations
that involve heavy lifting
Pathophysiology:
• Muscles play an important role in keeping the
abdominal organ in place.
• Increased intra-abdominal pressure with
presence of abdominal muscle weakness
allows a portion of intestine to push through
the abdominal wall.
• Intra-abdominal pressure may increase due to
lifting heavy objects, coughing, straining,
pregnancy, and tumor
Classification of Hernia:
• Reducible hernia: slips back into the
abdominal cavity with gentle pressure or
when the patient lies on his/her back.
• Irreducible hernia: is trapped and unable
to be replaced in a normal position, and
sometimes called incarcerated hernia
Types of Hernia:
Inguinal hernia.
Femoral hernia.
Umbilical hernia.
Ventral or incision hernia
Inguinal hernia
Femoral hernia
Umbilical hernia
Ventral or incision hernia
• Surgical repair of hernias is usually
recommended even if they are
reducible. Two surgical procedures
are used to repair hernias
1. Herniorrhaphy:
Surgical repair of the hernia through
ligation and removal of the hernia defect
2. Hernioplasty:
Surgical repair of the hernia with
reinforcement
of
the
weakened
musculature with fascia or a Dacron mesh.
Hernioplasty & Herniorrhaphy
Peritonitis
• Inflammation of peritoneum lining
• Enteric bacteria enter the peritoneal cavity
through a break of intact GI tract (e.g. perforated
ulcer, ruptured appendix)
• Causes include:
 Ruptured appendix
 Perforated bowel secondary to DU
 Gangrenous gall bladder
 Ulcerative colitis
 Trauma
 Peritoneal dialysis
Pathophysiology
• Peritonitis results from contamination of
normal sterile peritoneal cavity with infections
or chemical irritant
• Release of bile or gastric juices initially causes
chemical peritonitis; infection occurs when
bacteria enter the space
• Bacterial peritonitis usually caused by these
bacteria (normal bowel flora): Escherichia coli,
Klebsiella, Proteus, Pseudomonas
• Inflammatory process causes fluid shift into
peritoneal space leading to hypovolemia, then
septicemia
Manifestations
• Depends on severity and extent of infection,
age and health of client
• Presents with “acute abdomen”
-Abrupt
onset
of
diffuse,
severe
abdominal pain
- Pain may localize near site of infection
(may have rebound tenderness)
- Intensifies with movement
• Entire abdomen is tender with board like
guarding or rigidity of abdominal muscle
• Decreased peristalsis leading to
paralytic ileus, bowel sounds are
diminished or absent with progressive
abdominal distention, pooling of GI
secretions lead to nausea and
vomiting
• Systemically:
fever,
malaise,
tachycardia
and
tachypnea,
restlessness, disorientation, oliguria
with dehydration and shock
Diagnostic Tests
• WBC with differential: elevated WBC to
20,000
• Blood cultures: identify bacteria in blood
• Liver and renal function studies, serum
electrolytes: evaluate effects of peritonitis
• Abdominal x-rays:
detect intestinal
distension, air-fluid levels, free air under
diaphragm (sign of GI perforation)
• Diagnostic paracentesis
Medications
• Antibiotics
1.Broad-spectrum before definitive culture results
identifying specific organisms causing infection
2.Specific antibiotics treating causative pathogens
• Analgesics Intravenous
• fluids and electrolytes to maintain vascular
volume and electrolyte balance with NPO
• Bed rest in Fowler’s position to localize infection
and promote lung ventilation
• Intestinal decompression with nasogastric tube
or intestinal tube connected to suction
Surgery
• Laparotomy to treat cause (close
perforation, removed inflamed tissue)
• Peritoneal Lavage: washing out peritoneal
cavity with copious amounts of warm
isotonic fluid during surgery to dilute
residual bacterial and remove gross
contaminants
• Often have drain in place and/or incision
left unsecured to continue drainage
Intestinal obstruction
• Normal function of the small and large
intestine depends on the presence of an open
lumen or passageway for the movement of
contents; as well as adequate circulation
and nervous innervations to sustain normal
peristalsis; any factors or condition that
either narrow that intestinal passageway or
interfere with peristalsis can result
intestinal obstruction.
Intestinal obstruction
Types of intestinal Obstruction
• Mechanical intestinal obstruction:
Which accounts for 90% of
intestinal obstruction
• Nonmechanical
Intestinal
obstruction
Mechanical obstruction
1. Adhesion: is the most common small bowel
obstruction after abdominal surgery for
unknown
reasons;
perhaps
related
to
inflammatory responses in the healing bowel.
2. Hernias: if the abdominal wall defect through
which the hernia protrudes becomes so tight that
the bowel segment becomes strangulated
3. Tumor or neoplasm
4. Valvulus:A twisting of the bowel upon it
self.
Non-mechanical
•
May result from neuro-muscular or vascular
disorder:
1. Paralytic illus: result a lack of neurogenic
impairment, It is a common temporary
problem after abdominal surgery; particularly
if the bowel has been handled.
2. Mesenteric vascular occlusion infarction:
The most common causes are emboli and
atherosclerosis of mesentic arteries
Clinical manifestation
Clinical
Small intestine
manifestation
Large intestine
onset
Rapid
Gradual
vomiting
Frequent
Rare
Pain
Colic & cramping
Cramping &
abdominal pain
Bowel
Intermittent feces
for short time
Absolute
constipation
Abd.
distension
Minimally
increased
Greatly increased
Diagnosis
• History and physical examination
• Abdominal X-rays show the presence of gas and fluid
in the intestine
• Barium enemas:
Are helpful in locating large intestinal obstruction but
not used when performing is suspected
• Colonoscopy
• Laboratory test: CBC, serum electrolyte, blood urea
nitrogen then stool should be checked for occult
blood
Hemorrhoids
• Are enlarge veins located within tissues of
the lower portion of the rectum or anus.
Types of hemorrhoid
1. External hemorrhoids :Occur below the anal
sphincter. And can be detected by the affected
person. consists of small lumps of fibrous tissue
and folds of anal skin that been stretched
bulging of the hemorrhoid.
2. Internal hemorrhoids Those that occur above
the anal sphincter. Are not directly apparent to
the person unless they become so large that
they prolepses through the anus
Surgical management
• Sclerotherapy :The injection method can
be effective for small, bleeding internal
hemorrhoids. A sclerosing solution such as
5% phenol in oil is injected into the
sybmucous areolar tissue in which the
hemorrhoid vein lie. It consider palliative
and not curative, and injection may be
required in the future
• Cryosurgery: hemorrhoidectomy involves
freezing hemorrhoidal tissue through a probe
that carries liquid nitrogen are another agent
for a sufficient time to cause tissue necrosis
• Ligation: Internal hemorrhoid may be treated
by ligation with latex bands. The hemorrhoid
is grasped with forceps and pulled down into a
special instrument that, when the trigger
handle is pressed, slips a latex band over it.
The band constrict the circulation and cause
necrosis
• Hemorrhoidectomy
Cryosurgery & Ligation
Hepatitis
• The
word
"hepatitis"
means
inflammation of the liver and also
refers to a group of viral infections
that affect the liver. The most
common types are Hepatitis A,
Hepatitis B, and Hepatitis C
Types of Hepatitis
1.




Hepatitis A (HAV):
HBV is an RNA virus that transmitted
through the fecal oral route.
It frequently occurs in small outbreaks
caused by fecal contamination of food or
drinking water by an infected food handler.
It found in feces 2 or more weeks before the
onset of symptoms and up to 1 week after
the onset of jaundice.
The virus is present in feces during the
incubation period, so it can be carried and
transmitted
by
persons
who
have
undetectable, subclinical infections
2. Hepatitis B (HBV):
•
HBV is a DNA virus is transmitted by
Percutaneous
(e.g., IV drug use, accidental needle-stick punctures).
•
Permucosal exposure to:




Infectious blood, blood products:
Other body fluids (e.g., semen, vaginal secretions,
saliva) or other body fluids enter the body of a
person who is not immune to the virus.
Prenatal transmission from mother to infant can
occur. (Approximately 90% of infants infected at
birth go on to develop chronic hepatitis B.
The HBV can live-----------on a dry surface for at
least 7 days.
3.Hepatitis C Virus:
•
HCV is an RNA virus that is primarily
transmitted percutancously.
•
The major risk factor for infection is direct
percutaneous exposure, such as:
 Injecting drugs,
 Transfusion infected blood products,
 Hemodialysis,
 High-risk sexual behavior (e.g., unprotected
sex, multiple partners),
 Organ transplants, Exposure to blood and
blood products by health care workers
4. Hepatitis D Virus (Delta virus)
Is a defective single-stranded RNA
virus that cannot survive on its own.
HDV requires the help function of
HBV to replicate.
The importance of HDV relates to its
clinical virulence.
HDV infection can be acquired as a
co-infection with HBV
5.Hepatitis E Virus (HEV).





It is an RNA virus.
It transmitted by the fecal-oral route.
The most common mode of transmission
is drinking contaminated water.
It occurs primarily in developing
countries.
Epidemiology and clinical course similar
to those of hepatitis A virus infection;
enteric transmission
6.Hepatitis G Virus:
•
•
•
•
•
The HGV is an RNA virus.
Hepatitis G virus (HGV) is a recently
recognized although poorly characterized
parenterally and sexually transmitted virus.
Whether it accounts for all of the forms of
hepatitis that are not related to viruses A, B,
C, D, or E is not known.
It has been found in some blood donors and
can be transmitted by transfusion.
HGV often coexists with other hepatitis
viruses, such as HCV.
7. Autoimmune-Hepatitis:




This form of hepatitis is idiopathic; that
the cause is unknown.
Many of these patients often have a
number of systemic problems, including
glomerulonephritis and arthritis, the
disease is thought to be autoimmune.
The presenting signs and symptoms are
variable and similar to viral hepatitis.
Unlike viral hepatitis, autoimmune
hepatitis is treated with corticosteroids
or other immunosuppressive agents.
Hepatitis may be classified into
three phases
1. Preicteric or prodromal phase:
•
It precedes jaundice and lasts from 1 to
21 days. This is the period of maximal
infectivity for hepatitis (HAV).
•
Hepatitis B patients who are HBs Ag
positive and patients with HCV can be
infective for years
2. Icteric Phase:
•
•
•
•
It lasts 2 to 4 weeks and is characterized by
jaundice.
Jaundice results when bilirubin diffuses into
the tissues.
The urine may darken because of excess
bilirubin being excreted by the kidneys.
The stool will be light or clay colored, if
conjugated bilirubin cannot flow out of the
liver because of obstruction or inflammation
of the bile ducts.
3. Posticteric Phase:
•
•
•
•
The convalescent stage of the posticteric
phase
begins
as
jaundice
is
disappearing and lasts weeks to
months, with an average of 2 to 4
months.
During this period the patient’s major
complaint
is
malaise
and
easy
fatigability.
Hepatomegaly remains for several
weeks, but splenomegaly subsides
during this period.
Relapses
may
occur
and
the
disappearance of jaundice does not
mean the patient has totally recovered
Liver Cirrhosis
• Cirrhosis is a chronic progressive disease of the
liver characterized by extensive degeneration
and destruction of the liver parenchemal cells.
• Cirrhosis
refers
to
the
chronic,
degenerative changes (diffuse fibrotic
bands of connective tissue) which distort
the liver’s normal architecture. Extensive
degeneration
and
destruction
of
hepatocytes cell occur
Causes of Liver Cirrhosis:
Chronic hepatitis.
Repeated exposure to toxic substances.
Disease processes (such as sclerosing
cholangitis , cancer.
Chronic alcohol abuse. Alcohol abuse
accounts for most cases of cirrhosis.
The most common cause for cirrhosis in
Egypt is bilharaziasis
Types of Liver Cirrhosis
1.Laennec’ cirrhosis (most common type)
• It is also called as alcohol induced
nutritional or portal cirrhosis.
• Alcohol has a direct toxic effect on liver
cells (hepatocytes), causing inflammation.
• The liver enlarged, firm and hard in early
disease. The liver is smaller and nodular in
end-stage disease
2. Postnecrotic cirrhosis:
It caused by massive hepatic cell necrosis.
It is usually resulting from acute viral
hepatitis
or
exposure
to
certain
hepatotoxins such as industrial chemical
3.Biliary cirrhosis:
It caused by chronic billiard obstruction,
bile stasis, and inflammation.
The liver becomes fibrotic, hepatic cells
are destroyed.
4.Cardiac cirrhosis: / vascular cirrhosis:
• It caused by severe or chronic heart
failure.
• The liver becomes enlarged and
congested with venous blood resulting in
cell necrosis from anorexia
Complications of Cirrhosis:
•
•
•
•
•
•
Portal hypertension.
Bleeding esophageal varices.
Ascites.
Coagulation defects.
Jaundice
Portal –Systemic Encephalopathy (PSE)
with hepatic coma: It is basically a disorder
of protein metabolism and excretion
Jaundice & Ascites
ASSESSMENT AND MANAGEMENT OF
GASTROINTESTINAL DISORDERS
1.
•
•
•
Assessment: Done through the following
History (Health assessment interview)
Physical examination
Diagnostic tests
1. History (Health assessment interview)
–
–
Biographical and demographic data,
Current health ; chief complain & symptoms
focus on:
o Nausea & vomiting, Indigestion, Diarrhea
o Abdominal pain
o Appetite and weight change
– Past health history
– Family health
– Drug-nutrient interactions.
2. Physical examination
• Inspect and palpate lips and oral mucosa
• intolerance of foods that are acidic, spicy, or fatty
• Regurgitation of acidic gastric juice; increased
symptoms
when bending over, lying down, or
wearing
tight clothing; difficulty swallowing.
• Abdominal
assessment including appearance,
bowel sounds, and Epigastric tenderness.
• Chest pain, dysphagia ,coughing or hoarseness
• Heartburn, presence of bright blood or “coffeegrounds” appearing material in vomitus
Drug-nutrient interactions
Drug class
Possible nutrient interactions
Antacids
Decreased absorption of calcium,
iron, magnesium, zinc
Antibiotics
Cephalosporins: increased vitamin K
depletion
Anticoagulants
Vitamin K antagonist
Anticonvulsants
Decreased folate and biotin
Antituberculosis
drugs
Interfere with metabolism of vitamin
B6 and B12
Cathartics
Nonrenal
losses
of
calcium,
potassium, water
CholesterolInhibition of fat digestion and
absorption
reducing drugs
Simvastatin: grapefruit juice may
increase drug level
Diuretics
Increased renal loss of potassium,
calcium, magnesium, and zinc
H2 blockers
Decreased vitamin B12 absorption
Monoamine
Interact with tyramine-containing
oxidase inhibitors foods (cheese, smoked fish, wine,
yeast)
2. Nursing management
Common Nursing diagnosis:
 Ineffective airway Clearance relate to oral
surgery
 Altered comfortable related to gastritis,
acidity as manifested by gastric pain
 Imbalanced nutrition: less than body
requirements related to pain as manifested by
anorexia.
 Impaired skin integrity related to colostomy
and surgical incision
 Deficient fluid volume related to bowel obstruction,
vomiting
 Disturbed sleep pattern related to upper GIT bleed
 Knowledge defect related to treatment & long term
consequences of GERD problems
 Excess fluid volume related to liver cirrhosis as
manifested by ascites
 Activity intolerance related to pain and
weakness as manifested by inability to perform
ADLs
 Risk for infection related to NGT
Ineffective airway Clearance relate to oral
surgery as manifested by dyspnea
• Out comes
 Patient will demonstrate an effective respiratory rate,
depth, clear airway and expanded chest
• Intervention
 Assess respiration for rate, depth, rhythm, and causes of
dyspnea
 Put patient in comfortable position
 Administer O2 as prescribed
 Apply suction frequently if patient on ventilator
 Assess ABG frequently
 Apply chest physiotherapy
 Assess secretion color, amount if patient have
productive cough
 Give patient prescribed medication in accurate dose,
route and rate.
• Evaluation
 Respiratory with normal range, depth with normal ABG
and dyspnea relived
 Patient become comfortable
Altered comfortable related to gastritis,
acidity as manifested by gastric pain
• Out comes
 Comfortable level maintain.
 No signs & symptoms of restless and irritable
• Intervention
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Use pain scale(0-10) to assessing pain
Assess culture and beliefs about pain & pain relief
Assess patient pain tolerance
Give prescribed analgesics
Try to keep patient in comfortable position
Eliminate exercise according to patient ability and
tolerance
• Evaluation
Patient
reports
adequate
control
Vital signs within normal
No restless or irritability
pain
Imbalanced nutrition: less than body requirements
related to removal of part of stomach as manifested by
weight loss.
• Out comes




Adequate nutrition
Body weight maintained within normal
Normal serum electrolyte
Wound healing improved
• Intervention
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Assess patient weight, general appearance
Daily weight and measure intake & output
Assess hemoglobin, hematocrit, serum albumin,
Assess wound healing
Prescribed medication giving for nausea, pain before
meals
 Provide patient with favorite foods or have family bring
home-prepared feed if patient able to eat to increase
patient nutrition intake
 Keep patient in clean environment away from offensive
odors.
 Keep patient away from spicy and irritant foods
• Evaluation
 Patient maintain adequate nutrition
 Body weight maintained
 Normal serum albumin and electrolyte
Impaired skin integrity related to colostomy and
surgical incision
• Out comes
 Good skin and stoma integrity
 No signs of infection, vital signs within normal
• Intervention
 Monitor stoma color it should be pink, beefy red, and
moist without cyanosis or bleeding and should extend
about 2-3 cm from the abdominal wall
 Assess stoma function
 Empty the push when it not too full to avoid leakage.
 Apply a protective skin barrier under the pouch to
prevent
 Report abnormal assessment findings such as poor
stoma color, bulging or retracted stoma, or rash around
the stoma.
 Teach patient to notify health care provider if there is a
change in the stoma or if a rash develops in the skin
surrounding the stoma.
 Assess patient knowledge of stoma care, what
medications to avoid e.g., laxatives
 Assess surgical incision for bleeding, redness and
drainage at least ever 4 hours.
 Change dressing as ordered to keep the incision clean
and dry to prevent wound infection
• Evaluation
 Stoma pink and moist
 No signs of wound infection.
Deficient fluid volume related to bowel obstruction,
vomiting
• Out comes
 Fluid balance maintained
 Vital signs within normal
 Skin moist, warm and pink
• Intervention





Assess frequent and amount of vomiting.
Monitor vital signs especially blood pressure.
Monitor and record intake & output.
Administer IV fluids as prescribed to replace fluid loss.
Assess skin color, temperature, and character at least
every 4 hours
 Measure abdominal girth at least every 8 hours to
determine increasing distention and possible fluid
sequestering
 Assess abdomen for bowel sounds and tenderness
• Evaluation
 Fluid balanced maintained
 No signs of dry skin, hypertensive
 Abdomen soft no increase in girth, bowel sound present.
Knowledge defect related to treatment & long term consequences
of GERD problems
• Out comes
 Able to verbalize lifestyle modification
 Understand the chronic nature of the disease & longterm consequences
 Aware of the disease complication & how to deal with it
• Intervention
 Teach the importance of eating 4-6 small meals a day &
to eliminate foods known to decrease lower esophageal
sphincter pressure or cause irritation
 Instruct patient to avoid lying down after meals
 Educate patient about medication regimen and possible
side effects to improve adherence to medication regimen
 Use pain scale (0-10) to quantify pain and discomfort.
• Evaluation
 Understand the chronic nature of the disease & longterm consequences
 Patient adapt to lifestyle modification
 Patient Aware of the disease complication & how to deal
with it
Activity intolerance related to pain and weakness as
manifested by inability to perform ADLs
• Out comes
 Patient will participate effectively in performing activity of
daily living
• Intervention

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


Assess patient ability to tolerate activity
Maintain balanced diet
Make schedule of activity according to patient ability
Monitor vital signs during activity
Maintain patient hygiene
• Evaluation
•
Patient able to perform ADLs
Risk for infection related to NGT
•
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•
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•
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Out comes
No signs of infection
Vital signs within normal
Intervention
Maintain low intermittent suction
Check placement every 4 hours.
Monitor skin integrity of nose for insertion site and
provide skin care.
Monitor bowel sounds
Mouth care at least every 2 hours.
Evaluation
No signs of infection found