GID.pptx

THE DIGESTIVE SYSTEM
↗The digestive system is ma
de up of the
↗alimentary canal (food passa
geway) and
↗accessory organs of digestio
n

↗GIsystem may be divided into two sections:
↗the upper GI tract and
↗the lower GI tract.
↗The upper GI tract begins at the mouth and en
ds at the jejunum.
↗The lower GI tract begins at the ileum and end
s at the anus.

↗Accessory structures include
↗the peritoneum
↗Liver
↗gallbladder, and
↗pancreas.

• The primary functions of the GI tract are diges
tion and distribution of food.

Mouth
↗ Food normally enters the GI syste
m at the mouth, where it is chew
ed before being swallowed.
↗ Food that contains starch underg
oes partial digestion when it mixe
s with the enzyme salivary amylas
e, which the salivary glands secre
te.

Esophagus
↗The esophagus begins at the base of the phary
nx and ends at the opening to the stomach.
↗Layers of muscle tissue surround the esophag
us.

↗They consist of
↗striated muscle tissue in the proximal esophagus,
↗striated and smooth muscle in the mid-esophagus, and
↗smooth muscle in the lower esophagus.
↗Coordinated movement of these muscle layers propels
food into the stomach.
↗These wavelike contractions are known as peristalsis.
↗An upper esophageal sphincter or hypopharyngeal sph
incter prevents food or fluids from re-entering the pha
rynx

Stomach
↗The stomach temporarily holds ingested food
and prepares it by mechanical and chemical ac
tion to pass in semiliquid form into the small i
ntestine.
↗The opening between the esophagus and sto
mach is called the lower esophageal
sphincter or cardiac sphincter.

↗The opening between the stomach and duode
num is called the pyloric sphincter.
↗Both sphincters are circular bands of muscle fi
bers.
↗When contracted, these sphincters keep stom
ach contents enclosed (or confined).
↗When the pyloric sphincter relaxes, stomach c
ontents flow to the duodenum.

↗Gastric secretions that contain digestive enzym
es are released continuously but increase when
food is eaten.
↗Gastric secretions are acidic because they cont
ain hydrochloric acid (HCl).

• The contractions of the stomach mix the food
with the gastric secretions and move the mixt
ure of semiliquid food, called chyme
• The time required for the stomach to empty d
epends on the amount and composition of foo
d.
• Fats, for example, delay stomach emptying.

Small Intestine
↗The small intestine is divided into three portio
ns:
↗duodenum
↗jejunum, and
↗ileum.

↗ The duodenum, which is approximately
10 inches long, is the first region of the small intesti
ne and the site where bile and pancreatic enzymes e
nter.
↗ These secretions continue to promote the chemical
breakdown of food and transform chyme to an alkali
ne state.

↗The jejunum and ileum have a combined lengt
h of approximately 23 feet.
↗The primary function of the small intestine is t
o absorb nutrients from the chyme.
↗Absorption of different nutrients
occurs at different sites in the small intestine

↗When a part of the small intestine is diseased or rem
oved surgically, absorption in that area is diminished
or lost altogether.
↗The ileocecal valve lies at the distal end of the small i
ntestine and regulates the flow of intestinal contents,
which are liquid at this point, into the large intestine.
↗It also prevents the reflux of bacteria from the large i
ntestine, preserving the relative sterility of the small i
ntestine.

Large Intestine
↗The large intestine, approximately 4 to 5 feet long an
d 2 inches in diameter, receives waste from the small
intestine and propels waste toward the anus, the ope
ning from the body for elimination.
↗The large intestine absorbs water, some electrolytes,
and bile acids.
↗The cecum, colon, rectum, and anal canal make up th
e structures of the large intestine through which feca
l material passes.

↗The cecum is a pouch like structure at the begi
nning of the large intestine.
↗The appendix, a narrow blind tube at the
tip of the cecum, has no known function in hu
mans

↗The colon is divided into
the ascending, transvers
e, descending, and sigmo
id colons and rectum.

↗In the colon, the unabsorbed material become
s fecal matter, which is composed of water, fo
od residue, microorganisms, digestive secretio
ns, and mucus.
↗Water is reabsorbed by means of diffusion acr
oss the intestinal membrane as the mixture m
oves through the colon

↗The rectum holds and retains fecal matter
through the contraction of the internal and ex
ternal anal sphincters.
↗As fecal mass accumulates, it distends the rect
al wall, creating the urge to defecate.
↗When the external anal sphincter relaxes, the
fecal matter is expelled through the anus.

↗If any portion of the large intestine becomes d
iseased or is surgically removed, its absorptive
function is diminished or lost.
↗This may result in the passage of loose stools
and potential fluid and electrolyte imbalance.

↗Passage of liquid stool, which contains many b
ile salts, makes the client especially vulnerable
to skin breakdown in the perianal area.
↗If stool remains in the large intestine too long,
constipation results.
↗The client may then strain to evacuate hard, s
olid stool, which can disrupt skin integrity.

Accessory Structures
↗The three accessory digestive organs are the
↗Liver
↗gallbladder, and
↗pancreas.

Liver
↗ The largest glandular organ in the body, weigh
s between 1 and 1.5 kg.
↗It is located in the right upper abdomen just u
nder the diaphragm, which separates the
liver from the right lung.
↗The liver is involved in many vital, complex me
tabolic activities.

↗It forms and releases
↗Bile
↗processes vitamins, proteins, fats, and carbohydrates
↗Stores glycogen
↗contributes to blood coagulation
↗metabolizes and
↗biotransforms many chemicals (including drugs), bacteria,
and foreign matter; and
↗forms antibodies and immunizing substances

Gallbladder
↗The gallbladder is attached to the midportion of
the undersurface of the liver.
↗It normally has a thin wall and holds
approximately 60 mL of bile.
↗The liver forms approximately 1 L of bile each da
y.

↗When the bile reaches the gallbladder
from the common hepatic duct, water and mi
nerals are absorbed from the bile to form a m
ore concentrated product.

↗Gallbladder contraction, triggered by ingested food (
especially fats), causes bile to be released first throug
h the cystic duct and then the common bile duct into
the duodenum, where it aids in the absorption of fat
s, fat-soluble vitamins, iron, and calcium.
↗Bile also activates the pancreas to release its digestiv
e enzymes and an alkaline fluid that neutralizes stom
ach acids that reach the duodenum.

Pancreas
 The pancreas is both an exocrine gland, and an endo
crine gland.
 As an endocrine organ, it produces the hormones ins
ulin and glucagon
 As an exocrine organ, it produces various protein-, fat
-, and carbohydrate-digesting enzymes.

ASSESSMENT
• Many conditions can disrupt the normal function of the GI syst
em.
• In addition to disorders of the GI tract and accessory organs, m
any disorders involving other organ systems can affect GI functi
on.
• As a result, the client with a GI disorder may experience a wide
variety of health problems that involve disturbances of ingestio
n, digestion, absorption, and elimination.

• Accurate recording of the client’s health histor
y and physical assessment findings helps the h
ealthcare team to diagnose and treat GI disord
ers.

Nursing Assessment
When obtaining the nursing history of a gastrointesti
nal patient, a detailed interview should be conducte
d.
• Nursing personnel should question the patient abou
t his
– dietary habits
– bowel habits, and
– GI complaints (signs and symptoms).

Obtaining a history of dietary habits will provide valuab
le information.
Question the patient about the following:
• The number of meals ate per day.
• Meal times.
• Food restrictions or special diets followed.
• Changes in appetite. Increased? Decreased? No appetite?
• What foods, if any, have been eliminated from the diet? Why?
• What foods are not well tolerated?
• Alterations in taste.
• Medications used. Dosage and frequency.

Cont …
• Question the patient about
the following:
• Frequency of bowel movem
ents.
• Use of laxatives and/or ene
mas.
• Changes in bowel habits.
• Stool Description.
– Constipation.
– Diarrhea.
– Blood in stool.
– Mucous in stool.
– Black, tarry stools.
– Pale or clay colored stool
s.
– Foul smelling stools.
– Pain with stool.
Information about bowel patterns, especially a ch
ange in bowel patterns, can provide clues that will
aid in the diagnosis of the problem.

Cont…
 Ask the patient to describe any complaints not yet discussed in th
e interview.
 For example.
• Nausea. Frequency? Duration? Associated with meals? Relieved b
y?
• Vomiting. Frequency? Character of emesis? Relieved by?
• Heartburn/indigestion. Frequency? Duration? Associated with spe
cific foods? Relieved by?
• Gas (belching and flatus). Frequency? Associated with specific foo
ds? Relieved by?
• Weight loss. How much? In what time period?

Pain: Location? Frequency? Dura
tion? Character of the pain?
What does pain feel like?
Steady pain inflammatory pro
cess
Crampy pain obstructive proc
ess
Sharp (peritoneal irritation)
Dull peritoneal stretching

• Was onset of pain gradual
or sudden
• Sudden
– Perforation
– Hemorrhage
– Infract
• Gradual
– Peritoneal irritation
– Hollow organ distension
–

Does pain radiate?
• Right shoulder
– Gall bladder
• Around flank to groin
– Kidney, ureter
• Middle of back
– Pancreas

 Perform a brief, general head-to-toe visual inspection of th
e patient. Is height and weight within normal range for the
patient's age and body type?
 Observe the skin for the following:
• Color (pale, gray, ruddy, jaundiced).
• Bruises.
• Rashes.
• Lesions.
• Turgor and moisture content.
• Edema.

Cont…
 Examine the mouth and throat.
• Look at the lips, tongue, and mucous membranes
– noting abnormalities such as
• Cuts
• sores, or
• discoloration.
• Observe the condition of the teeth, Note any
– discolored,
– Cracked
– Chipped
– loose, or
– missing teeth.

• Observe the gums. Are they healthy and pink?
Note the patient's
– breath for unusual odors
• Fruity
• Foul
• alcohol, and
• so forth).

EXAMINATION OF THE ABDOMEN
 Physical examination of the abdomen involves visual inspection, ausc
ultation, and palpation.
• It is best to perform this examination while the patient is resting in a
– supine position
– knees slightly flexed to relax the abdominal muscles.
 In order to facilitate the referencing of location, the abdomen is view
ed as four quadrants or nine regions.

 Begin the abdominal examination by visually inspecting the ab
domen. Observe the following:
• Color.
– Pale?
– Jaundiced?
– Reddish ?
• Pigmentation. Even? Note blotches or lines of pigmentation.
• Contour. Symmetrical? Flat? Rounded? Sunken? Distended?
• Presence of: Petechiae? Scars? Rash? Visible blood vessels?
• Hair growth patterns.

 Next, auscultate the abdomen.
 Move the stethoscope in a symmetrical pattern, listening in all f
our quadrants.
• Listen for bowel sounds.
– The best location is below and to the right of the umbilicus.
• Describe the sounds heard according to location, frequency, an
d character of the sound.
• Abnormalities include absent bowel sounds and the peristaltic
rush of a hyperactive bowel.

 After auscultation, palpate the abdomen.
 Palpation is used to detect
 muscle guarding
 tenderness, and
 masses.
 Gently palpate the abdomen, moving in a symmetrical pattern
and covering all four quadrants.
 Record any of the following findings, noting the location.
• Rigidity or Guarding. This is the inability to relax the abdomin
al muscles.
• Pain or Tenderness. Ask the patient to describe the pain if palp
ation elicits a painful or tender area.

Rebound Pain.
This is pain felt upon release of pressure, as oppose
d to application of pressure.
Masses.
Organs can be palpated for size and contour by a trai
ned examiner. Additionally, masses and irregularities
in and around the abdominal organs may be detecte
d.

Diagnostic Tests
Various studies, both radiographic and nonrad
iographic, are used to identify the
location and structural appearance of
organs or
other space-occupying masses (air, fluid, tumors,
foreign objects) in the abdomen, or GI system.

The digestive tract can be outlined by x-rays
• The contrast medium is swallowed by the patient in or
der to visualize the upper GI tract.
• These procedures are referred to as "barium swallow,"
"upper GI," or "small bowel follow-through."
• To visualize the lower GI tract, the contrast medium is i
nstilled rectally.
• This procedure is called a "barium enema."

Pre-Procedural Nursing Implications.
 For upper GI examinations, the patient is normally
held NPO after midnight the day before the exam i
n order to empty the upper GI tract.
 Additionally, gum chewing and smoking should be
discouraged the morning of the exam, as this stimu
lates gastric action.

For lower GI tract examinations, the patient's l
arge intestine must be free of stool.
This is normally accomplished through the use
of laxatives and cleansing enemas.
The patient is held NPO after midnight the day
before the exam.
 The patient must be educated about the proc
edure, the significance of the preparation, and
any significant post-procedural sequelae.

 Post-Procedural Nursing Implications.
 Many patients experience constipation as a side eff
ect of the contrast medium.
 If so, mineral oil or a laxative may be required to relieve c
onstipation.
 Observe the patient for any signs of abdominal or r
ectal discomfort.
 Resume diet and medications as directed by surgeo
n

 Stool exam
• For
– unseen blood (occult)
– fat
– Urobilinogen
– Ova
– parasite
– bacteria, and
– other substances.

 Endoscopy is a visual examination of th
e interior through the use of special ins
truments called endoscopes.
• In relation to the digestive system, the
term endoscopy is used to describe vis
ual examination of the inside of the GI t
ract.
• Generally, the scope consists of a hollo
w tube with a lighted lens system that p
ermits multi-directional viewing.
• The scope has a power source and acce
ssories that permit both biopsy and suc
tion.

Pre-Procedural Nursing Implications.
• Endoscopic procedures are invasive, and therefore require a formal, signed co
nsent form.
• The patient must be educated about the procedure, the significance of any pr
eparation, and any post-procedural sequelae.
• Upper GI endoscopy requires that the patient be fasting.
• Sedatives are administered prior to the procedure to relax the patient and faci
litate passage of the scope.
• The physician may require the removal of the dentures prior to oral insertion
of the scope.
• Colon endoscopy requires that the bowel be free of stool to enhance visualiza
tion.
– This is normally accomplished with laxatives and cleansing enemas.

Post-Procedural Nursing Implications.
 Accidental perforation of the esophagus or colon may occur during endoscop
y.
 If pain or bleeding occur following the procedure, notify the professional nur
se. Note the following:
 Mouth or throat pain.
 Rectal pain.
 Abdominal pain.
 Bleeding from rectum.
 Bleeding from mouth or throat.
 Withhold foods, fluids, and p.o. medications until the patient is fully alert an
d gag reflex has returned.
 Take vital signs as indicated.

• Endoscopic examination of the
entire large bowel
• Liquid diet for 12 to 24 hr befor
e procedure, NPO for 6 to 8 hr
before procedure
• Bowel cleansing routine
• Assessment of vital signs every
15 min

• Endoscopic examination of the rectum and sig
moid colon
• Liquid diet 24 hr before procedure
• Cleansing enema, laxative
• Position client on left side in the knee-chest p
osture.

Cont…
• Mild gas pain and flatulence from air instilled i
nto the rectum during the examination
• If biopsy was done, a small amount of bleedin
g possible

Other Tests
• Ultrasonography
• Endoscopic ultrasonography
• Liver-spleen scan

Management of patient with upper gastro
intestinal disorder

Disorder of mouth and relate
d structure

Disorders of the Teeth
DENTAL PLAQUE AND CARIES
• Tooth decay is an erosive process that begins
with the action of bacteria on fermentable car
bohydrates in the mouth, which produces acid
s that dissolve tooth enamel

Dental Caries: A Bacterial Infection
• There are two specific groups of bacteria found in the
mouth that are responsible for dental caries:
– Mutans streptococci (Streptococcus mutans)
– Lactobacilli
• They are found in relatively large numbers
in the dental plaque.
• The presence of lactobacilli in the mouth indicates a h
igh sugar intake.

Dental Plaque
• Dental plaque is a colorless, soft, sticky coatin
g that adheres to the teeth.
• Plaque remains attached to the tooth despite
movements of the tongue, water rinsing, wate
r spray, or less than thorough brushing.
• Formation of plaque on a tooth concentrates
millions of microorganisms on that tooth.

The Caries Process
• For caries to develop, three factors must o
ccur at the same time:
– A susceptible tooth
– Diet rich in fermentable carbohydrates
– Specific bacteria (regardless of other factors, c
aries cannot occur without bacteria)

• The extent of damage to the teeth depends on
the following:
– The presence of dental plaque
– The strength of the acids and the ability of the sali
va to neutralize them
– The length of time the acids are in contact with th
e teeth
– The susceptibility of the teeth to decay

• Dental decay begins with a small hole, usually
in a fissure (a break in the tooth’s enamel) or i
n an area that is hard to clean.
• Left unchecked, the affected area penetrates t
he enamel into the dentin.

The earliest sign of decay is decalcification

Severely decayed molar on a child

Decay on the lingual of a maxillary lateral incisor

• Because dentin is not as hard as enamel, deca
y progresses more rapidly and in time reaches
the pulp.
• When the blood, lymph vessels, and nerves ar
e exposed, they become infected and an absce
ss may form, either within the tooth or at the t
ip of the root.

• Soreness and pain usually occur with an absce
ss.
• As the infection continues, the patient’s face
may swell, and there may be pulsating pain.
• The dentist can determine by x-ray studies the
extent of damage and the type of treatment n
eeded.

Management
• Treatment for dental caries includes:
– Fillings
– dental implants, and
– If treatment is not successful, the tooth may need
to be extracted.
• In general, dental decay is associated with you
ng people, but older adults are subject to deca
y as well, particularly from drug-induced or ag
e-related oral dryness.

Prevention
• Measures used to prevent and control dental c
aries include:
– practicing effective mouth care
– reducing the intake of starches and sugars (refined
carbohydrates),
– applying fluoride to the teeth or drinking fluoridat
ed water
– refraining from smoking and
– Controlling diabetes

Gerontologic Considerations
Oral Problems
• Many medications taken by the elderly cause
dry mouth, which is uncomfortable, impairs co
mmunication, and increases the risk of oral inf
ection
– These medications include the following:
• Diuretics
• Antihypertensive medications
• Anti-inflammatory agents
• Antidepressant medications

DENTOALVEOLAR ABSCESS
OR PERIAPICAL ABSCESS
• Periapical abscess, more commonly referred t
o as an abscessed tooth, involves the collectio
n of pus in the apical dental periosteum (fibro
us membrane supporting the tooth structure)
and the tissue surrounding the apex of the to
oth

• The abscess has two forms:
– acute and
– chronic.

• Acute periapical abscess is usually secondary t
o a suppurative pulpitis (a pus-producing infla
mmation of the dental pulp) that arises from a
n infection extending from dental caries.
• The infection of the dental pulp extends throu
gh the apical foramen of the tooth to form an
abscess around the apex.

• Chronic dentoalveolar abscess is a slowly progres
sive infectious process.
• It differs from the acute form in that the process
may progress to a fully formed abscess without th
e patient’s knowing it.
• The infection eventually leads to a “blind dental a
bscess,” which is really a periapical granuloma.
• It may enlarge to as much as 1 cm in diameter.
• It is often discovered on x-ray films and is treated
by extraction

Clinical Manifestations
• The abscess produces a dull, gnawing, continuous
pain, often with a surrounding cellulitis and edem
a of the adjacent facial structures, and mobility of
the involved tooth.
• The gum opposite the apex of the tooth is usually
swollen on the cheek side.
• Swelling and cellulitis of the facial structures may
make it difficult for the patient to open the mout
h.
• In well-developed abscesses, there may be a syst
emic reaction, fever, and malaise.

Management
• In the early stages of an infection, a dentist or de
ntal surgeon may perform a needle aspiration or
drill an opening into the pulp chamber to relieve t
ension and pain and to provide drainage.
• Usually, the infection will have progressed to a pe
riapical abscess.
• Antibiotics may be prescribed.
• After the inflammatory reaction has subsided, the
tooth may be extracted or root canal therapy perf
ormed.

Disorders of the Salivary Glands
• The salivary glands consist of the
• parotid glands, one on each side of the face below the ear
• submandibular and
• Sublingual glands, both in the floor of the mouth; and
• buccal gland, beneath the lips.
• About 1200 mL of saliva are produced daily.
• The glands’ primary functions are
– Lubrication
– protection against harmful bacteria, and
– digestion.

PAROTITIS
• Parotitis(inflammation of the parotid gland)
• is the most common inflammatory condition o
f the salivary glands
• Mumps (epidemic parotitis), a communicable
disease caused by viral infection and most co
mmonly affecting children
• is an inflammation of a salivary gland, usually t
he parotid.

– Elderly
– acutely ill, or
– debilitated people
• with decreased salivary flow from general dehydr
ation or medications are at high risk for parotitis.
• The infecting organisms travel from the mouth th
rough the salivary duct.
• The organism is usually Staphylococcus aureus (e
xcept in mumps).

Management
• Treat the underlying cause
• Analgesic for pain
• Adequate nutrition and fluid intake
• Good oral hygiene, and
• discontinuing medications that can diminish s
alivation may help prevent the condition.
– (eg, tranquilizers, diuretics)

SIALADENITIS
• Sialadenitis(inflammation of the salivary glands
• may be caused by
– Dehydration
– radiation therapy
– Stress
– malnutrition,
– Salivary gland calculi (stones), or
– improper oral hygiene.
– The inflammation is associated with infection by S. aur
eus, Streptococcus viridans, or pneumococcus.

• Symptoms include pain, swelling, and purulen
t discharge.
• Antibiotics are used to treat infections.
• Massage, hydration, and corticosteroids frequ
ently cure the problem.
• Chronic sialadenitis with uncontrolled pain is t
reated by surgical drainage of the gland or exci
sion of the gland and its duct.

What is an ulcer?
• A mouth or oral ulcer is an open sore in the
mouth, or rarely a break in the mucous memb
rane or the epithelium on the lips or surroundi
ng the mouth.

Epidemiology and frequency
• Mouth ulcer is a very common oral lesion.
• Epidemiological studies show an average prevalence bet
ween 15% and 30%.
• Mouth ulcers tend to be more common in women and th
ose under 45.
• The frequency of mouth ulcers varies from fewer than 4 e
pisodes per year to more than one episode per month in
cluding people suffering from continuous recurrent aphth
ous stomatitis

What cause ulcers?
• Trauma (physical injuries)
• Chemical injuries
• Smoking
• Infection
– viral
– Bacterial
– Fungal
– protozoans
• Immunodeficiency
• Autoimmunity
• Allergy
• Dietary

Tools for diagnosis:
• History
• Examination
• Further investigation
• Additional diagnostic methods – biopsy

Traumatic lesions
• Mechanical trauma (acute or chronic)
• Chemical injury (acid, alcali)
• Physical injury (thermal injury, electrical injur
y)

Mechanical trauma
• Can be:
1. Acute
2. Chronic

caused by:
1. A sharp edge of a tooth
2. Accidental biting
3. Sharp, abrasive,or exces
sively salty food
4. Poorly fitting dentures
5. Dental braces
6. Trauma from a tooth bru
sh

Acute trauma
• Single,
• can identify the cause
• should improve after re
moval

Clinical features of traumatic ulcers:
 They are clinically diverse, but usually appear as a single, pain
ful ulcer with a smooth red or whitish-yellow surface and a thi
n erythematous halo.
• They are usually soft on palpation, and heal without scarring
within 6–10 days, spontaneously or after removal of the cause
.
• However, chronic traumatic ulcers may clinically mimic a carci
noma.
• The tongue, lip, and buccal mucosa are the sites
• The diagnosis is based on the history and clinical features.
• However, if an ulcer persists over 10–12 days a biopsy must be
taken to rule out cancer.

Treatment
1. Removing factors, caused trauma
2. Good hygiene of oral cavity
3. Antiseptic for 7-10 days
4. Analgetics if it is necessary
5. Topical steroids may be used for a short time
.
6. Biopsy

Leukoplakia
• Etiology:
-trauma from habitual biting, den
tal appliances
-tobacco use
-alcohol consumption
-oral sepsis
-local irritation
-syphilis
-vitamin deficiency
-endocrine disturbances
-actinic radiation (in the case of li
p involvement).
• Symptoms –
– painless
– fuzzy white patches on the side of
the tongue or cheeks.

Clinical manifestation
• located on the tongue, mandibular alveolar ridge and buccal mucosa in
~50%.
• palate, maxillary alveolar ridge, lower lip, floor of the mouth and the re
tromolar regions are somewhat less frequently involved.
• may vary from nonpalpable, faintly translucent white areas to thick, fis
sured, papillomatous, indurated lesions.
• surface is often wrinkled or shriveled in appearance and may feel roug
h on palpation.
• color may be white, gray, yellowish-white, or even brownish-gray in pat
ients with heavy tobacco use.
Physical:
-lesion cannot be wiped away with a gauze

Differential diagnosis:
1. Candidiasis and aspirin burn - can be wiped a
way with a gauze

Treatment
• Treat dental causes such as rough teeth, irregu
lar denture surface, or fillings as soon as possi
ble.
• Stopping tobacco or/and alcohol.
• Removal of leukoplakic patches with using a
scalpel, a laser or an extremely cold probe tha
t freezes and destroys cancer cells (cryoprobe)
.

Chemical injures:
• Chemicals such as aspiri
n or alcohol that are held
or that come in contact w
ith the oral mucosa may c
ause tissues to become n
ecrotic and slough off cre
ating an ulcerated surface
.

Treatment:
1. Wash a mouth with lot of water
2. Analgesics
3. Antiseptics
4. Remove the cause

Physical injures:
• Electric Burns to the Mouth –
• are most commonly caused w
hen a child bites into a cord, i
mproperly connected cord,

Treatment:
1. Conservative
• Antiseptics
• Antibiotics
• Analgetic
2. Surgical

Stomatitis
• Definition
• Inflammation of the mucous lining of any of the structu
res in the mouth, which may involve the
– Cheeks
– Gums
– Tongue
– lips, and
– roof or
– floor of the mouth.
• The word "stomatitis" literally means inflammation of t
he mouth.

• The inflammation can be caused by conditions
in the mouth itself, such as
– poor oral hygiene
– poorly fitted dentures, or
– from mouth burns from hot food or drinks, or
– by conditions that affect the entire body, such as
medications, allergic reactions, or infections.

Herpetic stomatitis
• Herpetic stomatitis is a vir
al infection of the mouth
that causes ulcers and infl
ammation.
• These mouth ulcers are n
ot the same as canker sor
es, which are caused by a
different virus.

Symptoms:
• Blisters in the mouth, often on the tong
ue, cheeks, palate, gums, and a border
between the lip (red colored) and the n
ormal skin next to it
• Decrease in food intake, even if the pati
ent is hungry
• Difficulty swallowing (dysphagia)
• Fever (often as high as 104 °Fahrenheit)
may occur 1 - 2 days before blisters and
ulcers appear
• Irritability
• Pain in mouth
• Swollen gums
• Ulcers in the mouth, often on the tongu
e or cheeks -- these form after the blist
ers pop

Causes
• Herpetic stomatitis is a contagious viral illness caused b
y Herpes virus hominis (also herpes simplex virus, HSV).
• It is seen mainly in young children.
• This condition is probably a child's first exposure to the h
erpes virus.
• An adult member of the family may have a cold sore at th
e time the child develops herpetic stomatitis.
• More likely, no source for the infection will be discovered
.

Treatment:
• Good oral hygiene
• Acyclovir not later than 48 hours!
• Analgesic
• Diet (no hot or pepper food)
• Antiseptics

Aphthous Ulcers
• the most common non tra
umatic ulcer that affect or
al mucosa.

• Aphthous ulcers are also kn
own as canker sores.
• They are painful, temporary
sores that may occur anywh
ere in the mouth.
• Usually, they show up in sev
eral places:
• On the inside of the lips
• Inside the cheeks
• On the tongue
• At the base of the gums

Etiology:
1. Immune system disorders
2. Other conditions cause similar sores:
• Blood and immune system diseases, includin
g HIV
• Vitamin and mineral deficiencies
• Allergies

Minor ulcers:
• Are the most commonly e
ncountered form
• Single, painful oval ulcer l
ess than 0,6 mm, covered
by a yellow fibrinous me
mbrane
• Last 7 to 10 days
• Periods of freedom from
disease – 2-3 weeks to ye
ar

Major ulcers:
• Lesions are larger: more than
10 mm
• More painful
• Persist longer that minor apht
hae
• One ulcer disappears, another
one starts
• Healing generally occurs in 6 w
eeks and longer
• Chronic stress, common diseas
e can cause

Herpetiform ulcers
• Recurrent crops of small u
lcers
• Healing generally occurs i
n 1 to 2 weeks
• Not preceded by vesicle a
nd exhibit no virus-infecte
d cells

Treatment:
• Oral hygiene
• Avoiding spicy food
• Oral rinsing with sodium bicarbonate
• Analgesics
• Antiseptics
• Anti – inflammatory agents
• Antimicrobial and corticosteroids

common oppurtunistic
oral mycotic infection
 develops in the presence of
one of several predisposing
factors
• immunodeficiency
• endocrine disturbances
• diabetes mellitus
• poor oral hygiene
• xerostomia
Candidiasis

 caused by Candida albicans
 infection with this organism
is usually superficial, affecting
the outer aspects of
oral mucosa or skin
Candidiasis

 in severely debilitated + immunocompromised patients
such as patients with AIDS
 infection may extend into alimentary tract (candidal
esophagitis
 bronchopulmonary tract
 and other organ system
Candidiasis

 Clinical Features
 most common form is
acute pseudomembranous
also known, as thrush
• young infants + elderly
are commonly affected
Candidiasis

 oral lesion of acute
candidiasis (thrush)
• white
• soft plaques that sometime
grow centrifugally + merge
• wiping plaques with gauze
sponge leaves a painful,
eroded, eryhtematous or
ulcerated surface
Candidiasis

 Chronic Erythematous
Candidiasis
• commonly seen on
geriatric individuals
• who wear complete
maxillary denture
Candidiasis

 Chronic Erythematous
Candidiasis
• bright red
• relative little
keratinization
Candidiasis

 Hyperplastic Candidiasis
• usually asymptomatic
• usually discovered on
routine oral
examination
Candidiasis

 Mucocutaneous Candidiasis
• long standing
• persistent candidiasis of
 oral mucosa
 skin
 vaginal mucosa
Candidiasis

 Mucocutaneous Candidiasis
• often resistant to treatment
• begins as a pseudomembranous
type of candidiasis
• soon followed by nail +
cutaneous involvement
Candidiasis

 Treatment
 majority of infections may
be simply treated with
topical applications of
nystatin suspension
• nystatin cream or
ointment often effective
when applied directly to
denture-bearing surface itself
Candidiasis

 Treatment
 topical applications of either
nystatin or clotrimazole
should be continued for at
least 1 week beyond
disappearance of clinical
manifestations of disease
Candidiasis

 Treatment
 Hyperplastic Candidiasis
• topical + systemic antifungal
agents may not be effective
at completely removing
lesions
 surgical management
may be necessary
Candidiasis

 Treatment
 Chronic Mucocutaneous
Candidiasis associated
with immunosuppression
• topical agents may not
be effective
Candidiasis

 Treatment
 Chronic Mucocutaneous
Candidiasis associated
with immunosuppression
• systemic administration
of medications:
 Ketoconazole
 Fluconazole
 Itraconazole
Candidiasis

Client with Oral Cancer
• Uncommon (5% of all cancers) but has high rat
e of morbidity and mortality
• Highest among males over age 40
• Risk factors include
– smoking and using oral tobacco,
– drinking alcohol,
– marijuana use,
– occupational exposure to chemicals,
– viruses (human papilloma virus)

Pathophysiology
• Begin as painless oral ulceration or lesion with irregul
ar, ill-defined borders
• Lesions start in mucosa and may advance to involve t
ongue, oropharynx, mandible, maxilla
• Non-healing lesions should be evaluated for maligna
ncy after one week of treatment

Collaborative Care
• Elimination of causative agents
• Determination of malignancy with biopsy
• Determine staging with CT scans and MRI
• Based on age, tumor stage, general health and client’s pr
eference, treatment may include surgery, chemotherapy,
and/or radiation therapy
• Advanced carcinomas may necessitate radical neck dissec
tion with temporary or permanent tracheostomy; Surger
ies may be disfiguring
• Plan early for home care post hospitalization, teaching fa
mily and client care involved post surgery, refer to Americ
an Cancer Society, support groups

Gastroesophageal Reflux Disease (GERD)
• Gastroesophageal reflux is the backward flow of gastri
c content into the esophagus.
• GERD common, affecting 15 – 20% of adults
• 10% persons experience daily heartburn and indigesti
on

Pathophysiology
• Gastroesophageal reflux results from transient relaxation or in
competence of lower esophageal sphincter, sphincter, or incre
ased pressure within stomach
• Factors contributing to gastroesophageal reflux
1. Increased gastric volume (post meals)
2. Position pushing gastric contents close to
gastroesophageal juncture (such as bending or lying down)
3. Increased gastric pressure (obesity or tight clothing)
4. Hiatal hernia

Manifestations
• Heartburn after meals, while bending over, or recumbent
• May have regurgitation of sour materials in mouth, pain with s
wallowing
• Atypical chest pain
• Sore throat with hoarseness
• Bronchospasm and laryngospasm

Diagnostic Tests
• Barium swallow (evaluation of esophagus, stomach, s
mall intestine)
• Upper endoscopy: direct visualization; biopsies may
be done

Medications
• Antacids for mild to moderate symptoms
• H2-receptor blockers: decrease acid production; given B
ID or more often, e.g. cimetidine, ranitidine, famotidine,
nizatidine
• Proton-pump inhibitors: reduce gastric secretions, prom
ote healing of esophageal erosion and relieve symptoms
, e.g. omeprazole (prilosec); lansoprazole (Prevacid) initi
ally for 8 weeks; or 3 to 6 months
• Promotility agent: enhances esophageal clearance and g
astric emptying, e.g. metoclopramide (reglan)

Gastroesophageal Reflux Disease
Dietary and Lifestyle Management
• Elimination of acid foods (tomatoes, spicy, citrus foods, coffee
)
• Avoiding food which relax esophageal sphincter or delay gastri
c emptying (fatty foods, chocolate, alcohol)
• Maintain ideal body weight
• Eat small meals and stay upright 2 hours post eating; no eatin
g 3 hours prior to going to bed
• Elevate head of bed
• No smoking
• Avoiding bending and wear loose fitting clothing

Surgery indicated for persons not improved by
diet and life style changes
• Laparoscopic procedures to tighten lower eso
phageal sphincter
• Open surgical procedure
Nursing Care
• Pain usually controlled by treatment
• Assist client to institute home plan

Hiatal Hernia
Definition
• it is a protrusion of a portion of a stomach through a
diaphragmatic opening to the thoracic cavity
Predisposing factors include:
– Increased intra-abdominal pressure
– Increased age
– Trauma
– Congenital weakness
– Forced recumbent position

Hiatal Hernia
• Most cases are asymptomatic; incidence increases wi
th age
• There are two types of hiatal hernia:
– Sliding (direct esophageal hernia)
– Rolling (para esophageal hernia)

Hiatal Hernia
Sliding hiatal hernia: gastroesophageal junctio
n and fundus of stomach slide through the eso
phageal hiatus
The most common type of hiatal hernia (90%)

Hiatal Hernia
Paraesophageal hiatal hernia: the gastroesophageal j
unction is in normal place but part of stomach hernia
tes through esophageal hiatus; hernia can become st
rangulated; client may develop gastritis with bleeding

Cause
weakness of the muscle due to
• Age > 50 yrs.
• Injury with bullet [trauma]
• Thorax bullet operation
• IIAP[ Increased intra abdominal pressure]

Hiatal Hernia
Manifestations: Similar to GERD
• dysphagia
• chest discomfort
• Heart burn
• Regurgitation.
Diagnostic Tests
• Barium swallow
• Upper GI endoscopy

Hiatal Hernia
Treatment
• symptomatical RX.
• Elevate head of bed.
• Antacid
• Limitation of activity which increase intra abdominal pressure
• Dietary => small frequent diet
• Avoid irritant substance
Surgical mgt – If there is cxn.
_ If medical Rx- failed.

Hiatal Hernia
Complication
• obstruction
• Hemorrhage
• Aspiration

ACHALASIA
• It is a chronic progressive motor disorder of th
e lower 2/3 of esophagus.
• It is characterized by
– ineffective peristalsis and
– in effective dilatation

ACHALASIA
cause
• unknown
• but due to ineffective innervations
• dysphagia at early solid then soft or liquid diet
• filling full ness in the chest
• halitosis [fitted odor]
• regurgitation
• Wt-loss due to malnutrition

ACHALASIA
DX
• X- ray,
• Barium swallow,
• Endoscopy
CXn –
• Perforation,
• Bleeding,
• aspiration

ACHALASIA
Management
• small frequent diet,
• Elevate HOB,
• Anti acid
• Correct if anemia
• Nitrate to dilate LES.
• Balloon dilation

Esophageal divertricular
• It is an out pouching of the mucosa and sub-m
ucosa of the esophageal wall via a weak portio
n of musculature
Types
1- Zenkers [pharyhgoesophagial]
• Most common
• Common in male in ratio 3=1
• Common in age > 60 yrs-

Esophageal divertricular
2-Midd esophageal
• not common and less acute
3-lower esophageal [ epiphrenic]
• less common and less acute
management
• surgical- diverticulectomy
Complication
• Aspiration,
• lung abscess,
• malnutrition

Esophageal Cancer
• Relatively uncommon malignancy with high mortality rate, usually
diagnosed late
• Squamous cell carcinoma
1.Most common affecting middle or distal portion of
esophagus
2.More common in African Americans than Caucasians
3.Risk factors cigarette smoking and chronic alcohol use
• Adenocarcinoma
1.Nearly as common as squamous cell affecting distal
portion of esophagus
2.More common in Caucasians
3.Associated with Barrett’s esophagus, complication of
chronic GERD and achalasia

Esophageal Cancer
• Progressive dysphagia with pain while swallowing
• Choking, hoarseness, cough
• Anorexia, weight loss
Collaborative Care: Treatment goals
• Controlling dysphagia
• Maintaining nutritional status while treating carcino
ma (surgery, radiation therapy, and/or chemotherapy

Esophageal Cancer
Diagnostic Tests
• Barium swallow: identify irregular mucosal patterns or narrow
ing of lumen
• Esophagoscopy: allow direct visualization of tumor and biopsy
• Chest xray, CT scans, MRI: determine tumor metastases
• Complete Blood Count: identify anemia
• Serum albumin: low levels indicate malnutrition
• Liver function tests: elevated with liver metastasis

Esophageal Cancer
Treatments: dependent on stage of disease, client’s conditi
on and preference
• Early (curable) stage: surgical resection of affected portio
n with anastomosis of stomach to remaining esophagus;
may also include radiation therapy and chemotherapy pri
or to surgery
• More advanced carcinoma: treatment is palliative and m
ay include surgery, radiation and chemotherapy to contro
l dysphagia and pain
• Complications of radiation therapy include perforation, h
emorrhage, stricture

Summery
• GI Assessment
• Diagnostic procedures
• Disorder of oral & related structure
• Disorder of esophagus

Management of patient with gastric and duode
nal disorders

Gastritis
Definition:
• It is inflammation of the gastric or stomach mucosa
• It is a common GI problem.
Types
• Acute Gastritis
• Chronic gastritis

Gastritis
Causes of acute gastritis
• food that is contaminated with disease-causing microorg
anisms or that is irritating
• Irritants include aspirin and other NSAIDS, corticosteroids
, alcohol, caffeine
• Ingestion of corrosive substances: alkali or acid
• Effects from radiation therapy, certain chemotherapeutic
agents
• A more severe form of acute gastritis is caused by the ing
estion of strong acid or alkali, which may cause the muco
sa to become gangrenous or to perforate.

Gastritis
Manifestations
• Mild: anorexia, mild epigastric discomfort, belching
• More severe: abdominal pain, nausea, vomiting, hem
atemesis, melena
• If perforation occurs, signs of peritonitis

Gastritis
Treatment
• NPO status to rest GI tract for 6 – 12 hours, reintrodu
ce clear liquids gradually and progress; intravenous fl
uid and electrolytes if indicated
• Non- irritant diet when symptom subsides.
• Neutralize acid or alkaline if it is the cause.
• If symptom persists IV fluid

GHRONIC GASTRITIS
• Chronic gastritis is prolonged inflammation of the
stomach.
Cause
• may be caused by either
– benign or
– malignant ulcer of stomach or
– by H-pylori.
• Chronic gastritis can be
– type A or
– type B

Chronic Gastritis
Type A Chronic Gastritis
• It is auto immune [ due to change of parietal cell anti
gen antibody]
• Fund’s and body are the site
• It is associated with pernicious anemia.

Chronic Gastritis
• Type B Chronic Gastritis
• more common and occurs with aging
• caused by chronic infection of mucosa by Helic
obacter pylori; associated with risk of peptic ul
cer disease and gastric cancer
• Affects the remaining part of the stomach i.e.
antrum or pylorus

Chronic Gastritis
• Type A Chronic gastritis
– Most of the time asymptomatic except symptom of pern
icious anemia
• Type B chronic gastritis
– Anorexia, Heartburn [pyrosis]
– belching
– Fulfilness, nausea and vomiting hematoemesis, sour test
is the mouth

Chronic Gastritis
Collaborative Care
• Usually managed in community
• Teach food safety measures to prevent acute gastritis
from food contaminated with bacteria
• Management of acute gastritis with NPO state and th
en gradual reintroduction of fluids with electrolytes a
nd glucose and advance to solid foods
• Teaching regarding use of prescribed medications, s
moking cessation, treatment of alcohol abuse

Chronic Gastritis
Diagnostic Tests
• Gastric analysis: assess hydrochloric acid secretion (less with c
hronic gastritis)
• Hemoglobin, hematocrit, red blood cell indices: anemia includ
ing 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 l
aser coagulation or sclerosing agent

Chronic Gastritis
Treatment:
• Chronic gastritis
– Modifying patient diet
– reduce stress
– Antibiotic for H. Pylori (metronidazole (Flagyl) and cl
arithomycin or tetracycline) and proton–pump inhibitor
– Vitamin B- complex

• ....ALIYI KMSNMSN for regular CNPUD.ppt

Cancer of Stomach
Incidence
• Worldwide common cancer, but less common in US
• Incidence highest among Hispanics, African Americans, Asian
Americans, males twice as often as females
• Older adults of lower socioeconomic groups higher risk
Pathophysiology
• Adenocarcinoma most common form involving mucus-produci
ng cells of stomach in distal portion
• Begins as localized lesion (in situ) progresses to mucosa; sprea
ds to lymph nodes and metastasizes early in disease to liver, lu
ngs, ovaries, peritoneum

Cancer of Stomach
Risk Factors
• H. pylori infection
• Genetic predisposition
• Chronic gastritis, pernicious anemia, gastric polyps
• Achlorhydria (lack of hydrochloric acid)
• Diet high in smoked foods and nitrates
Manifestations
• Disease often advanced with metastasis when diagnosed
• Early symptoms are vague: early satiety, anorexia, indigestion, vo
miting, pain after meals not responding to antacids
• Later symptoms weight loss, cachexia (wasted away appearance)
, abdominal mass, stool positive for occult blood

Cancer of Stomach
Diagnostic Tests
• CBC indicates anemia
• Upper GI series, ultrasound identifies a mass
• Upper endoscopy: visualization and tissue biopsy of l
esion

Cancer of Stomach
Treatment
Surgery, if diagnosis made prior to metastasis
• Partial gastrectomy with anastomosis to duodenum:
gastroduodenostomy
• Partial gastrectomy with anastomosis to jejunum: gas
trojejunostomy
• Total gastrectomy (if cancer diffuse but limited to sto
mach) with esophagojejunostomy

Cancer of Stomach
Complications associated with gastric surgery
Dumping Syndrome
• Occurs with partial gastrectomy; hypertonic, undigested chym
e bolus rapidly enters small intestine and pulls fluid into intest
ine causing decrease in circulating blood volume and increase
d intestinal peristalsis and motility
• Manifestations 5 – 30 minutes after meal: nausea with possibl
e vomiting, epigastric pain and cramping, borborygmi, and dia
rrhea; client becomes tachycardic, hypotensive, dizzy, flushed,
diaphoretic
• Manifestations 2 – 3 hours after meal: symptoms of hypoglyce
mia in response to excessive release of insulin that occurred fr
om rise in blood glucose when chyme entered intestine

Cancer of Stomach
Treatment: dietary pattern to delay gastric emptying and allow s
maller amounts of chyme to enter intestine
• Liquids and solids taken separately
• Increased amounts of fat and protein
• Carbohydrates, especially simple sugars, reduced
• Client to rest recumbent or semi-recumbent 30 – 60 minutes
after eating
• Anticholinergics, sedatives, antispasmodic medications may b
e added
• Limit amount of food taken at one time

Cancer of Stomach
• Nutritional problems related to rapid entry of food into the bowel and the
shortage of intrinsic factor
• Anemia: iron deficiency and/or pernicious
• Folic acid deficiency
• Poor absorption of calcium, vitamin D
Radiation and/or chemotherapy to control metastasic spread
Palliative treatment including surgery, chemotherapy; client may have gast
rostomy or jejunostomy tube inserted

Management of patient with intestinal an
d rectal disorders

Acute Inflammatory IntestinalDisorders
APPENDICITIS
• The appendix is a small, finger-like appendage about
10 cm (4 in) long that is attached to the cecum just b
elow the ileocecal valve.
• The appendix fills with food and empties regularly in
to the cecum.
• Because it empties inefficiently and its lumen is small
, the appendix is prone to obstruction and is particul
arly vulnerable to infection (ie, appendicitis).
196

APPENDICITIS
• the most common cause of acute abdomen
• About 7% of the population will have appendicitis at
some time in their lives; males are affected more tha
n females, and teenagers more than adults.
197

Pathophysiology
• The appendix becomes inflamed and edematous as a
result of either becoming kinked or occluded by a fec
alith (ie, hardened mass of stool), tumor, or foreign b
ody.
• The inflammatory process increases intraluminal pres
sure, initiating a progressively severe, generalized or
upper abdominal pain that becomes localized in the r
ight lower quadrant of the abdomen within a few ho
urs.
198

• Vague epigastric or periumbilical pain progresses to ri
ght lower quadrant pain and is usually accompanied
by a low-grade fever and nausea and sometimes by v
omiting.
• Loss of appetite is common.
• Local tenderness is elicited at McBurney’s point whe
n pressure is applied
• Rebound tenderness may be present.
199

• Pain on defecation suggests that the tip of the appen
dix is resting against the rectum; pain on urination su
ggests that the tip is near the bladder or impinges on
the ureter.
• Some rigidity of the lower portion of the right rectus
muscle may occur.
• Rovsing’s sign may be elicited by palpating the left lo
wer quadrant; this paradoxically causes pain to be fel
t in the right lower quadrant
• If the appendix has ruptured, the pain becomes mor
e diffuse;
200

Assessment and Diagnostic Findings
• Diagnosis is based on results of a complete physical e
xamination and on laboratory and x-ray findings.
• The complete blood cell count demonstrates an elev
ated white blood cell count.
• The leukocytecount may exceed 10,000 cells/mm3, a
nd the neutrophil count may exceed 75%.
• Abdominal x-ray films, ultrasound studies, and CT sca
ns may reveal a right lower quadrant density or locali
zed distention of the bowel.
202

Complications
• The major complication of appendicitis is perforation
of the appendix, which can lead to peritonitis or an a
bscess.
• Perforation generally occurs 24 hours after the onset
of pain.
• Symptoms include a fever of 37.7°C or higher, a toxic
appearance, and continued abdominal pain or tende
rness.
203

Medical Management
• Surgery is indicated if appendicitis is diagnosed.
• To correct or prevent fluid and electrolyte imbalance
and dehydration, antibiotics and intravenous fluids ar
e administered until surgery is performed.
• Analgesics can be administered after the diagnosis is
made.
• Appendectomy (ie, surgical removal of the appendix)
is performed as soon as possible to decrease the risk
of perforation.
204

Nursing Management
• Goals include relieving pain, preventing fluid volume
deficit, reducing anxiety, eliminating infection from t
he potential or actual disruption of the GI tract, main
taining skin integrity, and attaining optimal nutrition.
205

PERITONITIS
• is inflammation of the peritoneum, the serous memb
rane lining the abdominal cavity and covering the vis
cera.
• Usually, it is a result of bacterial infection; the organis
ms come from diseases of the GI tract or, in women,
from the internal reproductive organs
• Peritonitis can also result from external sources such
as injury or trauma (eg, gunshot wound, stab wound)
or an inflammation that extends from an organ outsi
de the peritoneal area, such as the kidney..
206

• The most common bacteria implicated are Escherichi
a coli, Klebsiella, Proteus, and Pseudomonas,
• Other common causes of peritonitis are appendicitis
, perforated ulcer, diverticulitis, and bowel perforatio
n. Peritonitis may also be associated with abdominal
surgical procedures and peritoneal dialysis.
207

Pathophysiology
• Peritonitis is caused by leakage of contents from abd
ominal organs into the abdominal cavity, result of infl
ammation, infection, ischemia, trauma, or tumor per
foration.
• Bacterial proliferation occurs. Edema of the tissues re
sults, and exudation of fluid develops in a short time.
• Fluid in the peritoneal cavity becomes turbid with inc
reasing amounts of protein, WBC, cellular debris.
• The immediate response of the intestinal tract is hyp
ermotility, soon followed by paralytic ileus with an ac
cumulation of air and fluid in the bowel.
208

• The early clinical manifestations of peritonitis frequently are
the symptoms of the disorder causing the condition.
• At first, a diffuse type of pain is felt.
• The pain tends to become constant,
localized, and more intense near the site of the inflammation.
• Movement usually aggravates it.
• The affected area of the abdomen becomes extremely tende
r and distended, and the muscles become rigid.
• Rebound tenderness and paralytic ileus may be present.
• Usually, nausea and vomiting occur and peristalsis is diminis
hed.
• The temperature and pulse rate increase, and elevation of t
he leukocyte count.
209

Assessment and Diagnostic Findings
• The leukocyte is elevated.
• The HB and HCT levels may be low if blood loss occu
rred.
• Serum electrolyte studies
• An abdominal x-ray is obtained, and findings may sh
ow air and fluid levels as well as distended bowel loo
ps.
• A CT scan of the abdomen may show abscess
• Peritoneal aspiration and culture and sensitivity studi
es
210

Complications
• generalized sepsis.
• Sepsis is the major cause of death from peritonitis.
• Shock may result from septicemia or hypovolemia.
• The inflammatory process may cause intestinal obstr
uction.
• The two most common postoperative complications
are wound evisceration and abscess formation.
211

Medical Management
• Fluid, colloid, and electrolyte replacement is the major focus o
f medical management.
• The administration of several liters of an isotonic solution is pr
escribed.
• Analgesics, Antiemetics, Intestinal intubation and suction assis
t in relieving abdominal distention peritonitis.
• Large doses of a broad-spectrum antibiotic are administered i
ntravenously.
• Surgical objectives include removing the infected material and
correcting the cause.
• Surgical treatment is directed toward excision (ie, appendix), r
esection with or without anastomosis
212

Nursing Management
• Ongoing assessment of pain, vital signs, GI function,
and fluid and electrolyte balance is important.
• The nurse reports the nature of the pain, its location
in the abdomen, and any shifts in location. Administe
ring analgesic medication and positioning the patient
for comfort are helpful in decreasing pain.
213

CHRONIC INFLAMMATORY BOWEL DISEASE
• Ulcerative colitis

Intestinal obstruction
• Defn- it is an interruption in the normal flow o
f the intestinal content along the intestinal tra
ct
• It can be in small intestine or large intestine
• It may be complete or incomplete
• It may be mechanical or functional

Type 1- mechanical obstruction
• It is physical block to the passage of intestine
• Occur in small intestine than large intestine
• The most common cause is adhesive following operation an
d hernia in non-operated
• Volvulus (section of intestine twists over the other)
• hematoma
• tumor
• intussusceptions[ invagination]
• foreign body= fecal or barium impaction can the other caus
es
• about 90% of intestinal obstruction is adhesive

2-Paralytic ileus
• Ineffective paralysis
• Due to toxic or traumatic disturbance of ANS
• There is no physical blockage or blood supply
but due to nerve supply
Cause -
• spinal cord injury
• Post operatively
• Peritonitis

3- Strangulation
• Most of the time as a complication of hernia.
• If the blood supply is blocked following obstru
ction
• Cardinal symptoms of intestinal obstruction
– abdominal distention
– no flatus / no defecation
– vomiting
– Colic [ crampy] abdominal pain]

DX
– HX
– abdominal x-ray
– Barium enema
– CBC
Mgt
– correction of fluid and electrolyte
– long tube decompression
– surgery depend on condition
– Antibiotic should be given before surgery
– Surgery

CXn
• DHN [dehydration]
• shock
• sepsis
• death

ABDOMINAL HERNIA
• hernia is a protrusion of organ or its content t
hrough a weakened muscle.
• Hernia is often called rupture
Predisposing factor
• defect of muscle
– congenital
– Trauma
– IIAP=> cough, sneezing, constipation, lifting heavy
things, obesity, pregnancy

Classification of hernia
By site
– Inguinal hernia -
• direct inguinal hernia
• Indirect inguinal hernia
• Direct inguinal hernia
– Hernia through abdominal wall
• Indirect inguinal hernia
– Hernia through spermatic cord
• Femoral – common in female
• Umbilical hernia – common in obese elderly
and multipara
• Ventral or incision hernia after surgery.

Classification of hernia
– By severity – reducible = Hernia that can return back
• Irreducible = Hernia that can not return back
• Incarcerated = irreducible associated with obstructi
on
• Strangulated = irreducible type but associated
• with obstruction secondary to blood supply blockag
e

• bulging over herniated area when in standing
position and disappear when supine
• strangulation
– pain vomiting
– fever
• P/E
• Abdominal X- ray.

Management
• Mechanically [reducible]
• truss – is an appliance with pad and belt that i
s held over hernia if the Pt. is not candidate fo
r surgery
• Treat factors that increase Intra abdominal pre
ssure

Management
• Surgery – Removing sac replace content to its pal
ace then suture layer of muscle and fascia which
is called herniorrhappy
• Complication
– bowel obstruction
Nx- mgt
• Achieve contort
• Relieve pain postoperatively
• Teach the pt to hold the part of hernia while cou
ghing & sneezing
• post operatively, Present infection

GID.pptx

Recommended

Recommended

More Related Content

Similar to GID.pptx

Similar to GID.pptx (20)

More from MohammedAbdela7

More from MohammedAbdela7 (20)

Recently uploaded

Recently uploaded (20)

GID.pptx