Gastrointestinal System

Disorders
Gastrointestinal System
 Assessment of the GIT
Nursing History : Subjective Data
1. General Data
a. presence of dental prosthesis, comfort of usage
b. difficulty eating or digesting
c. food nausea or vomiting
d. weight loss
e. pain – may be caused by distention or sudden contraction of
any part of the GIT
- specify the area, describe the pain
2. Specific data if symptoms are present
• situations or events that effect symptoms
• onset, possible cause, location, duration, character
of symptoms
• relationship of specific foods, smoking or alcohol to
 Assessment of the GIT

3. Normal pattern of bowel elimination

a. frequency and character of stool
b. use of laxatives, enemas
4. Recent changes in normal patterns
• changes in character of stool (constipation, diarrhea, or
alternating constipation and diarrhea)
• changes in color of stool
melena - black tarry stool (upper GI bleeding)
hematochezia – fresh blood in the stool (lower GI bleeding)
c. drugs /medications being taken
d. measures taken to relieve symptoms
 B. Physical Examination : Objective Data

a.) Mouth and Pharynx

1. lips – color, moisture, swelling, cracks or lesions

2. teeth – completeness (20 in children, 32 in adults), caries, loose
teeth, absence of teeth  impair adequate chewing
3. gums – color, redness, swelling, bleeding, pain
4. (gingivitis) mucosa – color (light pink)

 examine for moisture, white spots or patches, areas of bleeding, or

ulcers
 white patches – due to candidiasis (oral thrush)
 white plaques w/in red patches may be malignant lesions
• tongue – color, mobility, symmetry, ulcerations / lesions or nodules
• pharynx – observe the uvula, soft palate, tonsils, posterior
pharynx
 signs of inflammation (redness, edema, ulceration, thick
yellowish secretions), assess also for symmetry of uvula
and
b.) Abdomen

- assess for the presence or absence of tenderness, organ enlargement,

masses, spasm or rigidity of the abdominal muscles, fluid or air
in the abdominal cavity

Anatomic Location of Organs

RUQ – liver, gallbladder, duodenum, right kidney, hepatic flexure of colon

RLQ - cecum, appendix, right ovary and fallopian tube
LUQ – stomach, spleen, left kidney, pancreas, splenic flexure of colon
LLQ – sigmoid colon, left ovary and tube
Assessment of the GIT
 1. Inspection

 assess the skin for color, texture, scars, striae,

engorged veins, visible peristalsis (intestinal
obstruction), visible pulsations (abdominal aorta),
visible masses (hernia)
 assess contour (flat, protuberant, globular) abdominal
 distension, measure abdominal girth or circumference
at the level of umbilicus or 2-5 cm. below
 2. Auscultation

 presence or absence of peristalsis or bowel sounds

 Normoactive – every 5-20 secs.

 Hypoactive – 1 or 2 sounds in 2 mins.

 Absent – no sounds in 3-5 mins.
 peritonitis, paralytic ileus,

 Hyperactive – 5-6 sounds in less than 30 sec.

 diarrhea, gastroenteritis, early intestinal
obstruction
3. Percussion

 done to confirm the size of various organs

 to determine presence of excessive amounts of air or fluid
 Normal – tympany
 dullness or flatness – area of liver and spleen, solid
structure
4. Palpation – tumor
 to determine size of liver, spleen, uterus, kidneys – if enlarged
 determine presence and chac. of abdominal masses
 determine degree of tenderness and muscle rigidity (rebound
or direct)
c.) Rectum
 perineal skin and perianal skin
 assess for presence of pruritus, fissures,
external hemorrhoids, rectal prolapse
 Diagnostic Tests
A. Laboratory tests
1. Stool examination (fecalysis)
 Stool for occult blood
o GI bleeding
o No red meat, turnips, horseradish, steroids,
NSAIDS, iron
 Stool for Ova and parasites
 proper collection of specimen  should not be
mixed with water or urine, should be sent
immediately to the laboratory
 2. CEA (Carcinoembryonic antigen)

 (+) colon cancer and other forms of cancer

 it is useful as in indicator of the effects of therapy

  CEA - recurrence or spread of tumor

  effectiveness of therapy
 A blood sample is withdrawn or sent to laboratory
 3. Exfoliative Cytology

 Detect malignant cells

 Liquid diet
 UGI: NGT insertion – saline lavage
 LGI: laxative, enema, proctoscope
Radiologic Tests
 visualization of the GIT by barium swallow, upper GI
series or barium enema

 Barium – is a radiopaque substance that when

ingested or given by enema in solution, outlines the
passage ways of the GIT for viewing by x-ray or
fluoroscopy
 1. Barium swallow/UGIS

 for identification of disorders of esophagus, stomach,

duodenum – esophageal lesions, hiatal hernia, esophageal
reflux, tumors, ulcers, inflammation

 Pt. swallows a flavored barium solution and the

radiologist observes the progress of the barium through
the esophagus and take x-ray films
 NPO for 6-8 hrs
 Post procedure:
o Increase fluid intake
o Laxative
o Stool – white for 24-72 hrs.
o Observe for: impaction, distended abdomen,
 2. Barium Enema/LGIS

Purpose : to visualize the colon to detect tumors, polyps,

inflammation, obstruction

 Prep.
o low residue diet (1-2 days), clear liquid diet (evening
meal)
o Laxative, cleansing enema in AM

 Post
o Laxative or enema
o Same as UGIS
 Other Tests
a.) Gastric analysis
 to quantify gastric acidity Normal 1-5 mEq / L

 gastric acid : gastric cancer, pernicious anemia

 gastric acid : duodenal ulcer
Normal gastric acid : gastric ulcer

 NPO for 12 hours

 an NGT is inserted and gastric contents are aspirated,
connected to suction
 b.) Biopsy

 Upper GI biopsy – biopsy of the oral cavity or tongue, or

any lesion or ulcerated area

- local anesthesia  assess site for bleeding , give oral

hygiene
 Biopsy of stomach - done during endoscopy
 Rectal biopsy – biopsy of lesions, polyps, tumors of the
lower sigmoid colon, rectum and anal canal  during
sigmoidoscopy
- monitor for signs of bleeding
Endoscopy
 directly visualize the GIT by the use of a fiberscape
 fiberscope – has a thin, flexible shaft that can pass through and
around bends in the GIT, transmit light and the image can be seen
in the monitor
 Endoscopy
1. Upper GI endoscopy
 Esophagoscopy, Gastroscopy and Duodenoscopy
 To identify upper GI bleeding, gastric cancer, gastric ulcers,
duodenal ulcers
 useful in detecting tumor, hernia, esophageal strictures
Preparation :
o NPO 6-8 hrs prior to procedure
o Anticholinergics(atropine), are given
o sedatives
o Remove dentures
o Lidocaine spray – depress gag reflex
Place on left side lying position
Post-procedure :
o NPO until gag reflex returns (2-4 hrs.)
o monitor vital signs, assess for dyspnea, dysphagia, abdominal
 Endoscopy
2. Colonoscopy
 to visualize the colon
 useful to identify tumors, colonic cancer, colonic polyps
 not done when there is active bleeding or inflammatory disease
Preparation :
 clear liquid diet 24 hrs. before
 fleet or cleansing enema
 dulcolax tabs
 NPO 8 hrs. prior to procedure
 Position: left side, knees flexed
Post-procedure :
 provide rest, monitor VS (vasovagal response-  HR,BP)
 assess for sudden abdominal pain (perforation), fever, active
bleeding
 Endoscopy
3. Sigmoidoscopy – examination of sigmoid colon, rectum and anus
Proctoscopy – examination of rectum and anus

 used as a screening test for persons 40 yrs old and above, with
history of colonic cancer
 used for pt with lower GI bleeding or inflammatory disease

Preparation :
 light dinner and light breakfast -
 dulcolax tab.
 Fleet enema or cleansing enema
Post-procedure :
 provide rest period
 assess for sudden abdominal pain, bleeding
Alternative Feeding:
2. Enteral hyperalimentation- delivery of nutrients directly to
the GI tract.

• Short- term- esophagostomy; nasogastric tube

• Long- term- gastrostomy; jejunostomy

Indications of NGT:

• Gavage- to deliver nutrients; for feeding purposes

• Lavage- to irrigate the stomach

• Decompression- to remove stomach contents or air

 Dental caries
Introduction
• Definition: Dental caries means rotten or decayed teeth.
• According to WHO- Dental caries is a microbial multifactorial disease of calcified tissue
of teeth, characterized by demineralization of the inorganic portion and destruction of
organic content.
MICROBIOLOGY
• Bacteria involved :
• • Streptococci e.g. mutans, sobrinus
• • Lactobacilli e.g. Acidophilus
Cariogenic properties of bacteria
• They are able to produce acid rapidly from fermentable carbohydrates
(acidogenic).
• They thrive under acid conditions (aciduric).
• Produce extracellular and intracellular polysaccharides which contribute to
the plaque matrix;
• Intracellular polysaccharides can be used for energy production and
converted to acid when sugars are not available
Various factors influencing the progression of caries
• Bacteria in dental plaque
• Substrate such as a fermentable carbohydrate (dietary sugars)
• A susceptible tooth surface
• Time
Role of plaque
• Plaque is an adhesive layer which deposits on the surface of the tooth and has
colonies of bacteria.
• It prevents the escape of acid into the saliva.
• It protects acid from buffering action of saliva due to its diffusion limiting
properties.
• In 2 weeks, the plaque is mature but there are considerable site-to-site
variations in its composition.
• Each site can be considered as unique and these local variations may explain
why lesions progress in some sites but not others in the same mouth.
• In the upper picture, a disclosing agent reveals the plaque, while in the lower picture the
plaque has been removed.
• White spot lesions are visible on the canines, but not on other tooth surfaces, although
plaque is present.
 Role of carbohydrate

The carbohydrate rapidly diffuse in the plaque and fermented to form acids there.
So, pH at the surface of tooth falls below critical level causing rapid demineralization of
enamel.
The plaque remains acidic for some time, taking 30–60 min to return to its normal pH in the
region of 7.
 A susceptible tooth surface
• Surface enamel is more resistant to caries than subsurface enamel.
• Surface enamel has high mineral content as fluoride, zinc, lead and iron.
• Hypoplastic enamel, deep narrow occlusal fissures, buccal or lingual pits
predispose tooth to develop caries.
 Susceptible tooth
• Attrition at occlusal surface causes lesser chance of caries.
• Rotated, mal-aligned, out of positioned, teeth are difficult to clean and
favour the development of caries.
• Under normal conditions, the tooth is continually bathed in saliva.
• It is capable of remineralizing the early carious lesion because it is
supersaturated with Ca and P.
• When salivary buffering capacity has been lost, a low Ph environment is
encouraged and persists for longer duration causing demineralization of
enamel.
Time
1. It is evident that the mere existence of the three factors operating
together does not result in instantaneous mineral loss.
2. Therefore a fourth circle is often added to stress the time dimension
taken for dental caries to develop.
 Other factors
• Age, Sex, Geography, Race, Economics status, Nutrition & Health status
Distribution of dental caries according to tooth surface:-
Occlusal > Interproximal >Buccal
Caries Susceptibility For Individual teeth
 Clinical Risk Assignment For Caries
• A patient is at high risk for the development of new cavitated lesions if:
• 1. High mutans streptococci (MS) counts are found.
• Bacteriologic testing MS should be done if:
• The patient has one or more medical health history risk factors.
• The patient has undergone antimicrobial therapy
• The patient presents with new incipient lesion
• The patient is undergoing orthodontic care
• The patient’s treatment plan calls for extensive restorative dental work
• 2. Any two of the following factors are present:
• Two or more active carious lesions
• Large number of restorations
• Poor dietary habits
• Low salivary flow
 Classification of Dental Caries
1. Clinical Classification
• According to the stage of lesion progression:
• Non cavitated lesion
• Cavity
• According to the severity of the disease:
• Acute caries (active)
• Chronic caries (slowly progression)
• Stabilized caries (arrested)
• According to clinical manifestation:
• White spot lesion macula caroisa
• Superficial caries caries superficialis
• Medium caries caries media
• Deep caries caries profunda
• Secondary caries caries secundaria
 2. ANATOMICAL

• According to anatomical depth of the defect:

• Enamel caries
• Dentin caries
• Cementum caries
• According to location of the lesion:
• Coronal caries
• Occlusal surfaces
• Smooth surfaces
• Approximal surfaces
• Root caries
• According to intensively of caries within the dentition:
• Single lesion
• Multiple lesions
• Systemic destruction
Cavitated lesion
 WHO classification
• The shape and the depth of the carious lesion can
• be scored on a 4 point scale:
• D1-Clinically detectable enamel lesions with intact
• (non-cavitated) surfaces.
• D2-Clinically detectable cavities limited to enamel.
• D3-Clinically detectable lesions in dentin (with
• and without cavitation of dentin).
• D4–Lesions into the pulp.
 Caries Diagnosis

Diagnosis is important for three reasons:

• It forms the basis for a treatment decision.
• Active lesions require some form of active management whereas arrested
lesions do not.
• Informing the patient.
• The patient is central to the management of the carious process.
• It is the patient who will control the process, not the professional.
• The dentist’s role is to inform the patient whether any action is required.
• Advising health service planners.
• Epidemiological surveys inform the politicians who commission them of the
state of health and disease of the population.
• These surveys should assist them to direct money appropriately.
 Diagnostic Methods

• 1. Identification of subsurface demineralization (inspection,

radiography, dye uptake methods).
• 2. Bacterial testing.
• 3. Assessing environmental conditions (pH, salivary flow, salivary
buffering).
Assessment Tools:
• Patient History.
• Clinical Examination.
• Nutritional Analysis.
• Salivary Analysis.
• Radiographic Assessment.
A past history of caries experience is the best predictor of future caries activity est
 5- Radiographic Assessment
• Although radiographs may show caries that is not visible clinically.
• The minimal depth of a detectable lesion on a radiograph is about
500 lam.
• Although radiographs tend to underestimate the histologic extent of
a carious lesion, approximately 60% of teeth with radiographic
proximal lesions in the outer half of dentin are likely to be
noncavitated.
• Thus, many lesions evident radiographically are not cavitated and
should be remineralized rather than restored.
 Caries Prevention
Goal
• To reduce the number of cariogenic bacteria.
• To limit tooth demineralization.
Preventive methods
• Limiting pathogen growth and metabolism.
• Increasing the resistance of the tooth surface to demineralization through the
following approaches
• General Health.
• Fluoride Exposure.
• Immunization.
• Salivary Function.
• Antimicrobial Agents.
• Diet.
• Oral Hygiene.
• Pit and Fissure Sealants.
• Restorations.
 Caries Treatment
• In the Past: Drill and Fill Approach
• In the Present: Early Detection and Remineralization
 Esophageal Disorders
Dysphagia

 problem in ingesting necessary nutrients because of difficulty in

swallowing
Causes :
1) pharyngeal muscle weakness
 disease or trauma of glossopharyngeal nerves
 neuromuscular disorders (poliomyelitis, multiple sclerosis,
myasthenia gravis
2) esophageal disorders
 obstruction caused by enlarged thyroid, tumors, strictures  narrowed
opening
 absence of peristalsis of the esophagus
Pathophysiology
Weak pharyngeal/esophageal muscles  difficulty moving the food from
the oropharynx into the esophagus
 immediate regurgitation of fluids into the nasal passages
 aspiration of feedings may occur from failure of the glottis to close
 Esophageal Disorders
Assessment

 history of difficulty in swallowing

 assess for gag reflex – touching the posterior tongue or pharynx
with a tongue depressor
 ask the pt to swallow and observe movement of the larynx
Nsg. Management
Pts. with pharyngeal weakness:
 can tolerate solids more easily than liquids
 teach “double-swallow” technique – 1) inhale, 2) put food pharynx
in and swallow 3) exhale 4) swallow again
 helps minimize the possibility of aspiration
 closely supervise the pt during feeding, suction equip. shld. be ready
 elevate head of bed during feeding or position on the unaffected
side
- to ensure better control
 if the ability to swallow is absent  NGT or gastrostomy
feeding weakness:
Pts. With esophageal
 small-frequent feedings are advised to pts
 elevate head of bed
 Gastroesophageal Reflux Disease (GERD)

 refers to a group of conditions that cause reflux of gastric and

duodenal contents back to the esophagus

Causes :
- idiopathic incompetent lower esophageal sphincter (LES)
- pregnancy
- obesity
- surgical removal lower esophagus due to cancer
- ascites
- hiatal hernia  major cause

Hiatal hernia – refers to protrusion of part of the stomach, through the

diaphragmatic hiatus into the thoracic cavity  caused by obesity, trauma,
weakening of muscles
 Gastroesophageal Reflux Disease (GERD)

Pathophysiology

Lower esophageal sphincter (LES) – muscle at the junction between

esophagus and stomach

 When food enters the pharynx and esophagus  LES relaxes to

permit or allow food to enter into the stomach
 LES is usually contracted to prevent reflux of gastric material
back to the esophagus
  LES pressure  reflux can occur
 caused by anticholinergics, caffeine, alcohol, smoking, when the person
is lying down
 Gastroesophageal Reflux Disease (GERD)

S/SX :

 heartburn (pyrosis) – major symptom of GERD

 burning sensation below the sternum that may be referred or
radiate to the back or neck if severe
 frequently accompanied by a sour regurgitation of gastric
contents into the mouth but is not accompanied by nausea

Hiatal hernia – may be diagnosed by x-ray, upper gastrointestinal series

(UGIS)
 Gastroesophageal Reflux Disease (GERD)

Medical Mgt.
Liquid antacids (ex. Maalox) – 30 ml taken 1 hr. and 3 hrs. after meals and
at bedtime or whenever heartburn occurs  to decrease gastric acidity
Medications that increase LES contraction
 Urecholine, Metoclopramide HCL (reglan, plasil)  to be taken 30
mins. before meals and at bedtime
 Cimetidine, Ranitidine, Famotidine (histamine H2 receptor –
blockers)
used for severe reflux, acts by reducing gastric secretions, thereby
Surgery for hiatal hernia
decreasing irritating effects
Ex. Posterior gastropexy – returning the stomach to the abdomen and
suturing it in place
Nissen fundoplication – wrapping the fundus of the stomach around
the lower part of the esophagus to restore sphincter competence and
prevent reflux
 Gastroesophageal Reflux Disease (GERD)

Nsg. Intervention
Patient teaching for GERD:
3.high-protein, low-fat diet ( to stimulate release of gastrin and
cholecystokinin   LES pressure)
4.avoidance of foods containing caffeine (coffee, tea, colas),
theobromine
(chocolate) and alcohol   LES pressure
5.small, frequent meals ( to prevent gastric distention with resulting
gastric acid secretion)
• smoking
6.avoidance of –: it  LES pressure
• supine position for 2-3 hrs after eating
• bending over ( intraabdominal pressure)
• lifting heavy objects and wearing tight belts or
girdles after
•sleepingeating ( to
with the prevent
head slightly abdominal
elevated  topressure)
prevent regurgitation while
pt is sleeping
Achalasia
 also called cardiospasm or aperistalsis
 there is absence of peristalsis in the esophagus and in
which the esophageal sphincter fails to relax after
 swallowing cause is unknown
 little or no food enters the stomach

S/Sx:
 gradual onset of dysphagia for both fluids and solids
 loss of weight
 substernal chest pain
 regurgitation of
esophageal contents
Diagnostic tests
onto : Barium
pillow swallow, esophagoscopy
at night
 Achalasia
Medical Mgt:
Medications – Nitrates, Nifedipine – to decrease LES pressure
Forceful dilation of the LES by pneumatic dilators  a balloon
inserted and inflated for is
- opens the sphincter and2-3
1 min., relieves
timesthe dysphagia

Nsg. Interventions:
encourage pt. to drink fluids with meals and use the valsalva
maneuver (bearing down with a closed glottis) while swallowing 
to help push the food
advise soft diet
elevate head during sleeping to prevent regurgitation
after esophageal surgery, monitor for signs of esophageal
perforation as evidenced by chest pain, shock, dyspnea and
fever
 Esophageal Strictures
 narrowing of the lumen of the esophagus
Causes :
ingestion of corrosive substances (alkaline or acid)
reflux esophagitis - prolonged NGT

irritation of the esophageal walls lead to formation of a stricture that 

the esophageal lumen and leads to dysphagia
food may collect and partially or totally obstruct the esophagus
fluids are easier to swallow than solids
Interventions :
gradual dilation by mechanical dilators or balloons
rubber or metal mechanical dilators of increasing sizes are passed through
the area of strictures, producing mild discomfort
the balloon is inflated to create pressure
dilation procedure is done every 3-4 wks for 4-6 months
monitor pt for signs of esophageal perforation
 Esophageal Carcinoma
 most common cause of obstruction of the esophagus
 Risk factors – chronic GERD, achalasia, smokers, alcoholics
 tumor occur commonly in the middle and lower third of
esophagus
 common type is squamous cell carcinoma, occur in ages 40-70
y.o
 early diagnosis and treatment is important for treatment
to be successful  report and consult to the doctor for
any sign of dysphagia
S/Sx
 progressive dysphagia – 1st solid food  then liquids
 regurgitation may occur, aspiration  coughing and
pneumonitis
 foul breath and foul taste in the mouth
 metastasis rapidly occurs to the pulmonary system,
 Esophageal Carcinoma

Medical Mgt.
Surgery :
o Esophagogastrostomy (removal of the lower part of the
esophagus and part of the stomach)
o Esophagectomy
o Radical neck dissection

Radiation and chemotherapy – done 3-4 wks before surgery,

reduces tumor size and facilitates surgery and length of
survival
 Esophageal Carcinoma
Nursing Management: Post-op care

 Fowler’s position – to prevent reflux

 observe for regurgitation and dyspnea

 prevent aspiration pneumonia – turn to sides

 NGT attached to low intermittent suction (for decompression); do

not manipulate bec. damage to the anastomosis may occur; removed after 5-
7 days.

 Feeding through tube jejunostomy

 Start oral feeding small sips of water  soft diet (after 1-2 wks)

 Remain upright for at least 2 hours after each meal

Antacids and metoclopramide - promote gastric motility

 Esophageal varices
• Esophageal varices are abnormal, enlarged veins in the tube that
connects the throat and stomach (esophagus).
• This condition occurs most often in people with serious liver
diseases.
• Esophageal varices develop when normal blood flow to the liver is
blocked by a clot or scar tissue in the liver.
• To go around the blockages, blood flows into smaller blood vessels
that aren't designed to carry large volumes of blood.
• The vessels can leak blood or even rupture, causing life threatening
bleeding.
• A number of drugs and medical procedures can help prevent and
stop bleeding from esophageal varices.
 Variceal pressure
• Measurement of the difference between intra-variceal pressure and pressure
within the esophageal lumen (the transmural pressure gradient across the
varices) is potentially a more important indicator of bleeding risk than
measurement of hepatic vein pressure gradient(HVPG).
• A miniature pneumatic pressure sensitivity gauge attached to the tip of an
endoscope allows noninvasive measurement of variceal pressure.
• A variceal pressure > 18 mm Hg during a bleeding episode is associated with
failure to control bleeding and predicts early rebleeding.
• Patients on pharmacologic therapy who show a decrease in variceal pressure of >
20% from baseline have a low probability of bleeding.
 Portal hypertension
• Portal hypertension is an increase in hepatic sinusoidal pressure to 6 mm Hg
or greater.
• Portal hypertension is directly responsible for the two major complications of
cirrhosis:
• variceal hemorrhage
• ascites.
• The development of gastroesophageal varices requires a portal pressure
gradient of at least 10 mm Hg.
• A portal pressure gradient of at least 12 mm Hg is thought to be required for
varices to bleed.
• Portosystemic collaterals decompress the hypertensive hepatic sinusoids and
give rise to varices at different sites.
• Variceal hemorrhage is an immediate life-threatening with a 20–30%
mortality rate associated with each episode of bleeding
 Pathophysiology of variceal formation

• Portal hypertension results from:

• Increase in portal resistance
• Increase in portal inflow.
• Dilated Collateral vessels forms new vascular sprouts that connects
the high-pressure portal venous system with lower-pressure systemic
veins.
• This process of angiogenesis and collateralization is insufficient for
normalizing portal pressure and leading to portal hypertension and
esophageal varices
 HEPATIC CIRCULATION
• SPLANCHNIC CIRCULATION: is the circulation of GIT originating at celiac trunk
(superior and inferior mesenteric artery)
• Vasodilatation, particularly in the splanchnic bed, permits an
increase in inflow of systemic blood into the portal circulation.

• Splanchnic vascular endothelial cells are primarily responsible for

mediating splanchnic vasodilatation and enhanced portal venous
inflow through excess generation of NO
• HEPATIC CIRCULATION
• The changes in portal flow and resistance also can be viewed as
originating from mechanical and vascular factors.
• Mechanical factors include the fibrosis and nodularity of the
cirrhotic liver.
• Vascular factors include intrahepatic vasoconstriction.
 Etiology
• Esophageal varices sometimes form when blood flow to your liver is blocked,
most often by scar tissue in the liver caused by liver disease.
• The blood flow begins to back up, increasing pressure within the large vein
(portal vein) that carries blood to your liver.
• This pressure (portal hypertension) forces the blood to seek other pathways
through smaller veins, such as those in the lowest part of the esophagus.
• These thin-walled veins balloon with the added blood. Sometimes the veins can
rupture and bleed.
• Causes of esophageal varices include:
• Severe liver scarring (cirrhosis).
• A number of liver diseases — including hepatitis infection, alcoholic liver
disease, fatty liver disease and a bile duct disorder called primary biliary
cirrhosis — can result in cirrhosis.
• Blood clot (thrombosis).
• A blood clot in the portal vein or in a vein that feeds into the portal vein
(splenic vein) can cause esophageal varices.
• A parasitic infection: Schistosomiasis can damage the liver, as well as the lungs,
intestine and bladder
 Risk factors
• Although many people with advanced liver disease develop esophageal varices,
most won't have bleeding.
Varices are more likely to bleed if:
• High portal vein pressure.
• The risk of bleeding increases with the amount of pressure in the portal vein
(portal hypertension).
• Large varices.
• The larger the varices, the more likely they are to bleed.
• Red marks on the varices.
• When viewed through an endoscope passed down your throat, some varices
show long, red streaks or red spots.
• These marks indicate a high risk of bleeding.
• Severe cirrhosis or liver failure.
• Most often, the more severe your liver disease, the more likely varices are to
bleed.
• Continued alcohol use. Your risk of variceal bleeding is far greater if you
continue to drink than if you stop, especially if your disease is alcohol related.
 Sign and Symptoms

• Esophageal varices usually don't cause signs and symptoms

unless they bleed.
• Signs and symptoms of esophageal varices bleeding include:
• Vomiting and seeing significant amounts of blood in your
vomit
• Black, tarry or bloody stools
• Lightheadedness
• Loss of consciousness (in severe case)
signs of liver disease includes:
• Yellow coloration of your skin and eyes (jaundice)
• Easy bleeding or bruising
• Fluid buildup in your abdomen (ascites)
 Complications

• The most serious complication of esophageal varices is bleeding.

• Once you have had a bleeding episode, your risk of another bleeding episode
greatly increases.
• If you lose enough blood, you can go into shock, which can lead to death.
Diagnosis
• Main tests used to diagnose esophageal varices are:
• Endoscope exam. A procedure called upper gastrointestinal endoscopy is the
preferred method of screening for varices. Your
• Imaging tests. Both abdominal CT scans and Doppler ultrasounds of the
splenic and portal veins can suggest the presence of esophageal varices.
 Treatment
• In emergency situations, care is directed at stopping blood loss, maintaining
plasma volume, correcting disorders in coagulation induced by cirrhosis, and
appropriate use of antibiotics such as quinolone or ceftriaxone.
• Blood volume resuscitation should be done promptly and with caution.
• The goal should be hemodynamic stability and hemoglobin of over 8 g/dl.
• Resuscitation of all lost blood leads to increase in portal pressure leading to
more bleeding.
• Volume resuscitation can also worsen ascites and increase portal pressure.
• Therapeutic endoscopy is considered the mainstay of urgent treatment.
• The two main therapeutic approaches are variceal ligation or banding and
sclerotherapy.
 Prevention

• Avoid alcohol
• Eat healthy diet
• Use chemicals sparingly
• Reduce risk of hepatitis
Gastric Disorders
 Structural Layers of the GIT
1. Mucosa – mucous membrane composed of three layers
a. Epithelium
b. Lamina propria – connective tissue containing blood vessels,
lymph nodes and glands:
 cardiac glands – secrete mucus
 chief (peptic) cells – secrete mucus and pepsinogen  pepsin
 parietal cells – secrete hydrochloric acid (HCL) and water, also
produce intrinsie factor
 neck cells - secrete mucus
 pyloric glands – secrete gastrin and mucus
• Muscularis mucosa – thin layer of smooth muscle between mucosa and
submucosa
• Submucosa – connective tissue containing blood vessels, lymph channels,
nerves and glands
• Tunica muscularis – layers of smooth muscle
 produce peristaltic activity of the stomach as it mixes food
during digestion
 Stomach
Gastric Secretion
 The stomach secretes 1500 to 3000 ml of gastric juice per day. Major
secretions are HCL, pepsin and mucus
 HCL and pepsin provide the corrosive power of gastric secretion
 Pepsin is the most active factor in the digestive processes of the
stomach, acting to break proteins into polypeptides
 Mucus has a neutralizing effect which protects the stomach mucosa

3 Phases of Gastric Secretion

1. Cephalic Phase
 is stimulated by hunger, food odors, sight and smell, taste
 it begins before food enters the stomach
 is mediated by the vagus nerve, releasing acetylcholine
stimulates
which the parietal cells and chief cells to secrete acid, pepsin and
mucus
 Gastric secretion
2. Gastric Phase
 begins with the arrival of food in the stomach
 distention of the stomach and presence of digested proteins
stimulate gastrin hormone secretion
 Gastrin stimulates the parietal cells of the stomach to
 this
secrete
phaseHCL
continues for several hours, until the acidity of gastric
contents reaches pH of 1.5

3. Intestinal Phase
 is stimulated by food entering the duodenum
 a substance similar to gastrin is released from the intestines  it
stimulates gastric secretion of pepsin and mucus
 when the pH in the duodenum decreases ( acidity) this results
to release of Secretin hormone – w/c inhibit gastric acid
secretion
and slows gastric motility and gastric emptying
 Acute Gastritis
 transient inflammation of the gastric mucosa
 char. by erosion of the surface epithelium in a diffuse
or localized pattern, that are usually superficial

Causes / precipitating factors :

 injury of the protective mucosal barrier by drugs or chemicals
 anti-inflammatory drugs ex. Aspirin, NSAIDs  inhibit
prostaglandin which normally stimulate mucus secretion
 steroids ex. Prednisone
 food or substance poisoning
 bacterial infection (staphylococcus organism)
 alcohol abuse
 extreme physical stress or prolonged emotional
 tension excessive amounts of coffee, tea, pepper,
 stimulate acid secretion
spices
 Acute Gastritis
Clinical Manifestations:
 epigastric pain or discomfort
 abdominal tenderness
 cramping
 severe nausea and vomiting
 eructation (belching /
 burping) anorexia
 sometimes gastrointestinal – hematemesis
bleeding
 Healing usually occurs spontaneously within a few days
Discontinuing injurious drugs, using antacids (ex. Maalox),
decreasing acid secretion using Histamine receptor (ex.
blockers
Ranitidine, Cimetidine) facilitates healing
Eat non-irritating
Provide bed rest bland diet ( avoid highly seasoned, greasy or
 Gastric Cancer

 May develop in any part of the stomach but is found commonly at the
distal third
 More common in men and in age 50-70 years old

Causes: heredity, chronic gastric ulcer, chronic gastritis

S/Sx:
 Gastric distress
 Flatulence
 Early satiety
 Loss of appetite, anorexia
 Loss of strength and weight loss
Dx: UGIS, absence of HCL – due to destruction of parietal cells by cancer
cells
Tx: Gastrectomy, chemotherapy
Gastric Cancer
 Colorectal Cancer
Definition
• a. Third most common cancer diagnosed
• b. Affects sexes equally
• c. Five-year survival rate is 90%, with early
diagnosis and treatment
Risk Factors
• a. Family history
• b. Inflammatory bowel disease
• c. Diet high in fat, calories, protein
Pathophysiology
• a. Most malignancies begin as adenomatous polyps and arise in
rectum and sigmoid
• b. Spread by direct extension to involve entire bowel
circumference and adjacent organs
• c. Metastasize to regional lymph nodes via lymphatic and
circulatory systems to liver, lungs, brain, bones, and kidneys
Manifestations
• a. Often produces no symptoms until it is advanced
• b. Presenting manifestation is bleeding; also change in bowel
habits (diarrhea or constipation); pain, anorexia, weight loss,
palpable abdominal or rectal mass; anemia
Colon Cancer
Complications
• a. Bowel obstruction
• b. Perforation of bowel by tumor, peritonitis
• c. Direct extension of cancer to adjacent organs;
reoccurrences within 4 years
Collaborative Care: Focus is on early detection and
intervention
Screening
• a. Digital exam beginning at age 40, annually
• b. Fecal occult blood testing beginning at age 50, annually
• c. Colonoscopies or sigmoidoscopies beginning at age 50,
every 3 – 5 years
Diagnostic Tests
• a. CBC: anemia from blood loss, tumor growth
• b. Fecal occult blood (guiac or Hemoccult testing): all colorectal cancers
bleed intermittently
• c. Carcinoembryonic antigen (CEA): not used as screening test, but is a
tumor marker and used to estimate prognosis, monitor treatment, detect
reoccurrence may be elevated in 70% of people with CRC
• d. Colonoscopy or sigmoidoscopy; tissue biopsy of suspicious lesions,
polyps
• e. Chest xray, CTscans, MRI, ultrasounds: to determine tumor depth,
organ involvement, metastasis

• Pre-op care
• Consult with ET nurse if ostomy is planned
• Bowel prep with GoLytely
• NPO
• NG
Surgery
• a. Surgical resection of tumor, adjacent colon, and regional
lymph nodes is treatment of choice
• b. Whenever possible anal sphincter is preserved and
colostomy avoided; anastomosis of remaining bowel is
performed
• c. Tumors of rectum are treated with abdominoperineal
resection (A-P resection) in which sigmoid colon, rectum, and
anus are removed through abdominal and perineal incisions and
permanent colostomy created
Colostomy
1. Ostomy made in colon if obstruction from tumor
• a. Temporary measure to promote healing of anastomoses
• b. Permanent means for fecal evacuation if distal colon and
rectum removed
2. Named for area of colon is which formed
• a. Sigmoid colostomy: used with A-P resection formed on LLQ
• b. Double-barrel colostomy: 2 stomas: proximal for feces
diversion; distal is mucous fistula
• c. Transverse loop colostomy: emergency procedure; loop
suspended over a bridge; temporary
• d. Hartman procedure: Distal portion is left in place and oversewn;
only proximal colostomy is brought to abdomen as stoma;
temporary; colon reconnected at later time when client ready for
surgical repair
 Postoperative care
• Pain
• NG tube
• Wound management
• Stoma
• Should be pink and moist
• Drk red or black indicates ischemic necrosis
• Look for excessive bleeding
• Observe for possible separation of suture securing stoma to abdominal wall
• Evaluate stool after 2-4 days postop
• Ascending stoma (right side)
• Liquid stool
• Transverse stoma
• Pasty
• Descending stoma
• Normal, solid stool
Radiation Therapy
• a. Used as adjunct with surgery; rectal cancer has high rate of
regional recurrence if tumor outside bowel wall or in regional
lymph nodes
• b. Used preoperatively to shrink tumor
• C. Provides local control of disease, does not improve survival
rates
Chemotherapy:
Used postoperatively with radiation therapy to reduce rate of
rectal tumor recurrence and prolong survival
 Nursing Care

• a. Prevention is primary issue

• b. Client teaching
• 1. Diet: decrease amount of fat, refined sugar, red meat; increase amount of
fiber; diet high in fruits and vegetables, whole grains, legumes
• 2. Screening recommendations
• 3. Seek medical attention for bleeding and warning signs of cancer
• 4. Risk may be lowered by aspirin or NSAID use
Nursing Diagnoses for post-operative colorectal client
• a. Pain
• b. Imbalanced Nutrition: Less than body requirements
• c. Anticipatory Grieving
• d. Alteration in Body Image
• e. Risk for Sexual Dysfunction
Home Care
• a. Referral for home care
• b. Referral to support groups for cancer or ostomy
• c. Referral to hospice as needed for advanced disease
Post-op Care