Care of Clients with

GASTROINTESTINAL
PROBLEMS
FLORENCE IVAN C. TUBBAN , RN
 OVERVIEW OF THE
ANATOMY AND
PHYSIOLOGY OF THE
GASTROINTESTINAL
SYSTEM
Functions of the Digestive System
Ingestion
• Taking food and water into the mouth
Breaking down of food
• Mechanical digestion: chewing, mixing, and
churning food
• Chemical digestion: digestive enzymes
breakdown food
Absorb nutrients
• Movement of nutrients from the GI tract to the
blood or lymph
Release of waste
• Elimination of indigestible solid wastes
The GIT is composed of 2 general parts:

ACCESSORY DIGESTIVE
MAIN GIT ORGANS

The digestive tract or The accessory digestive organs

gastrointestinal (GI) tract is a aid in the breakdown of
muscular tube that winds foodstuff
through the body and is
responsible for the digestion Teeth, tongue, gallbladder,
and absorption of food salivary glands, liver, and
pancreas
Oral cavity, pharynx,
esophagus, stomach, small
intestine, large intestine, and
anus
MOUTH

• Contains the lips, cheeks, palate, tongue, teeth,

salivary glands, masticatory/facial muscles and
bones
• Important for mechanical digestion of food
• Saliva contains SALIVARY AMYLASE or PTYALIN
that starts the initial digestion of carbohydrates
Parotid Glands: largest; anterior to each ear; serous
glands
Submandibular Glands: inferior portion of the
mandible; more serous than mucus secretions
Sublingual Glands: smallest; below the tongue;
primarily mucus secretions
 ESOPHAGUS
• A hollow muscular tube
• Length- 25 cm
• Made up of stratified squamous epithelium
• Located in the mediastinum, anterior to the
spine , posterior to the trachea and heart
• The upper third contains skeletal muscles, contains
the upper esophageal or hypopharyngeal sphincter
• The middle third contains mixed skeletal and
smooth muscles
• The lower third contains smooth muscles and the
esophago-gastric/ cardiac sphincter is found here
• Functions to carry or propel foods from the
oropharynx to the stomach
 STOMACH
• J-shaped organ in the LUQ
• Contains four parts- the fundus, the
cardia, the body and the pylorus
• The cardiac sphincter prevents the
reflux of the contents into the
esophagus (entrance)
• The pyloric sphincter regulates the rate
of gastric emptying into the duodenum
(exit)
• Capacity is 1,500 ml!
• The functions of the stomach are
generally to digest the food (proteins)
and to propel the digested materials
into the SI for final digestion
Glands and cells in the stomach secrete
digestive enzymes:
1. Parietal cells - HCl acid and Intrinsic
factor
2. Chief cells- pepsin = digestion of
PROTEINS!
3. Antral G -cells- gastrin
4. Argentaffin cells- serotonin
5. Mucus neck cells- mucus
 SMALL INTESTINE
- Longest segment, about 2/3 of the total length
- Grossly divided into the
Duodenum: (proximal)
Jejunum: (middle)
Ileum : (distal)
- Duodenum w/ampulla of Vater: common bile duct empties,
passage of bile and pancreatic secretions
- The ileum is the longest part (about 12
- The intestinal glands secrete digestive enzymes that
feet)
finalize the digestion of all foodstuff
- Body’s major digestive organ
- Digestion is completed and absorption occurs
- Enzymes for carbohydrates : disaccharidases
- Enzymes for proteins : dipeptidases and aminopeptidases
- Enzyme for lipids : intestinal lipase
2 Types of contractions in the small intestines
a. segmental contractions- mixing waves that move the intestinal contents back and forth in a
churning motion
b. intestinal peristalsis- propels the contents towards the colon
* both movements are stimulated by the presence of chyme ( distention)
- Finger like projections (villi) are present throughout the small intestines- absorption-begins in the
jejunum by active transport and diffusion

Segmentation contractions Peristalsis contractions

LARGE INTESTINE
• Approximately 5 feet long, and 6.5 cm(2.5 in.) in diameter,
extends from the ileum to the anus
• Contains cecum,appendix, colon, rectum and anal canal
• Cecum is the proximal end of large intestine where it joins
with the small intestine at the ileocecal junction
- Attached to the cecum is the appendix
• Colon consists of four parts: ascending colon, transverse
colon, descending colon and sigmoid colon
- Mucosal Lining of colon contains crypts
• Rectum is a straight muscular tube that begins at the
termination of the sigmoid colon and ends at anal canal
• Anal Canal is the last part of the digestive tract ; begins at
inferior end of rectum and ends at anus
-Forms internal anal sphincter and external anal
sphincter
Digestive Processes
• Chewing
- 1.5ml of saliva is secreted daily from the
parotid, submaxillary and sublingual glands
- PTYALIN or SALIVARY AMYLASE is an
enzyme that begins the digestion of starches
Digestive Processes

Swallowing begins as a voluntary act, w/c is

regulated by the swallowing center in the
medulla oblongata of the CNS

Swallowing occurs in three stages:

(1) Oral phase: voluntary stage: bolus is
passed into the oropharynx;
(2) Pharyngeal phase, the involuntary
passage of the bolus through the pharynx
into the esophagus
(3) Esophageal phase: involuntary passage
of the bolus through the esophagus
into the stomach.
 Digestive Processes

Gastric Function
- stomach: secretes a highly acidic fluid in response to the
presence of ingested food
- gastric fluid: 2.4L/day; pH as low as 1 and derives its acidity
from hydrochloric acid (HCL)
a. stimulates the secretion of hormones that promote the flow of
bile and pancreatic juice
b. to breakdown food into more absorbable components
c. to aid in the destruction of ingested bacteria
Gastric Enzymes
Secreted by zymogens or chief cells
Amylase=for starch digestion
Lipase=for fat digestion
Pepsin=for protein digestion
Rennin=for milk and protein digestion

Parietal cells
HCl - maintains acidity 1.0 pH destroy some
bacteria ingested aids also in digestion of food
Intrinsic factor - aids in absorption of vitamin
B12
* pernicious anemia
 Waste Products of Digestion
• Feces - undigested foodstuff, inorganic
materials, water and bacteria
• 75% fluid 25% solid material
• brown color results from the breakdown of
bile
• gases- methane, hydrogen sulfide and
ammonia
• Elimination begins with distention of the
rectum w/c initiates contractions of the
rectal musculature and relaxes the closed
internal anal sphincter
DEFECATION REFLEX
● occurs when feces distend the rectal
wall
● consists of local and
parasympathetic reflexes
● Local reflexes cause weak
contractions of the distal colon and
rectum.
● Parasympathetic reflexes cause
strong contractions, and are
normally responsible for most of the
defecation reflex.
• internal anal sphincter- autonomic
nervous system
• external anal sphincter- cerebral
cortex; maintained in tonic contraction
GASTROINTESTINAL
ASSESSMENT
 
LABORATORY PROCEDURES
Fecalysis
• Stool exam; Examination of stool consistency, color and the presence of
occult blood.
• Special tests for fat, nitrogen, parasites, ova, pathogens and others

WATERY STOOL may be due to:

 Cathartics
 Diarrhea, irritation
 Early typhoid (pea-soup)
 Cholera (rice water)
EXCESSIVELY HARD STOOL /
SCYBALOUS
 Prolonged constipation (ball shaped)
 Scybala – goat droppings due to small
bulk of feces and lack of moisture
E.g., spastic colitis, atony of colon
GASEAOUS / FERMENTIVE
 Soft, mushy, bulky, bubbles of gas (frothy)
 E.g., carbohydrate fermentation
FLATTENED / RIBBON-LIKE
 Pipestem
 E.g., spastic colitis, lower colon
obstruction
SMALL CALIBER
 Spasms, hemorrhoids, cancer, ulcer
LARGE CALIBER
 Constipation
 Hirschsprung’s disease
 FECALYSIS: Occult Blood Testing

- Aka : stool occult blood test,

hemoccult test, guiaic smear test,
gFOBT, or occult blood test
- Instruct the patient to adhere to a 3-day
meatless diet ; NO RED MEAT: (FALSE
POSITIVE)
- No intake of NSAIDS, aspirin and anti-
coagulant (FALSE POSITIVE RESULT)
- No vitamin C – FALSE NEGATIVE RESULT
- Screening test for colonic cancer
 Upper GIT study: Barium swallow test
- Examines the upper GI
tract
- swallowing study,
esophagography,
modified barium swallow
study, video fluoroscopy
swallow study
- Barium sulfate is usually
used as contrast
- Pre-test: NPO post-midnight
- Post-test: Laxative is
ordered, increase fluid
intake, instruct that stools
will turn white,
- Monitor for obstruction
 Lower GIT study: Barium enema
Examines the lower GI tract
 Gastric analysis

- Aspiration of gastric juice to measure pH,

appearance, volume and contents
- Pre-test: NPO 8 hours, avoidance of
stimulants, drugs and smoking
- Post-test: resume normal activities
EGD - esophagogastroduodenoscopy
● Visualization of the upper GIT by
endoscope
● Pre-test: ensure consent, NPO 8 hours,
pre-medications like atropine and
anxiolytics
Gastroscopy Intra-test:
easy access
position : LEFT lateral to facilitate salivary drainage and

● Post-test: NPO until gag reflex returns, place patient in SIMS position
until he awakens, monitor for complications, saline gargles for mild
oral discomfort
NURSING
IMPLICATIONS
FOR UPPER
ENDOSCOPY
 Lower GI- scopy
● Use of endoscope to visualize the anus, rectum, sigmoid and colon
● Pre-test: consent, NPO 8 hours, cleansing enema until return is
clear
● Intra-test: position is LEFT lateral, right leg is bent and placed
anteriorly
● Post-test: bed rest, monitor for complications like bleeding and
perforation
Anoscopy, proctoscopy,
and sigmoidoscopy
● Anoscopy requires the use of a rigid scope to
examine the anal canal; the client is placed in the
knee-chest or left lateral position.
● Proctoscopy and sigmoidoscopy require the use of
a flexible scope to examine the rectum and sigmoid
colon; the client is placed on the left side with the
right leg bent and placed anteriorly.
Colonoscopy A fiberoptic endoscopy study in which the lining of the large
intestine is visually examined; biopsies and polypectomies
can be performed
 ASSESSMENT AND
MANAGEMENT OF
PATIENTS WITH ORAL AND
ESOPHAGEAL DISORDERS

FLORENCE IVAN C. TUBBAN , RN

Conditions of the Oral
Cavity
Disorders of the Teeth
 Dental Plaque -aka ‘’tooth decay’' is an erosive process that begins w/ the action of bacteria on
fermentable CHO in the mouth, w/c produces acid that dissolve
and Caries -Streptococcus mutans—colonize the organic buffering biofilm (plaque) on the
tooth surface
extent of damage to the teeth CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
depends on the ff:
• presence of dental plaque: • fuzzy feeling on the teeth • Mouth Care: brushing and
gluey, gelatin-like substance • Chronic flossing, normal mastication
that adheres to the teeth bad breath (halitosis) (chewing), normal flow of
• strength of the acid and ability • Red, swollen, tender saliva
of the saliva to neutralize • Diet- ↓ the amount of sugar &
• the length of time the acids
gums that bleed after
starch
are in contact brushing • Fluoridation
• susceptibility of the teeth to • Pit and Fissure Sealants-
decay special coating to fill and seal
pits and fissures, can last to
5-10 years
Dentoalveolar abscess -more commonly referred to as an abscessed tooth
or Periapical Abscess -Collection of pus in the apical dental periosteum (fibrous membrane supporting
the tooth structure) and the tissue surrounding the apex (in the jaw bone)
May be acute or chronic CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Acute - secondary to a
suppurative pulpitis that arises • Dull, gnawing, continuous Break in Gingival Mucosa Diagnostics:
from an infection from a dental pain w/ surrounding -X-ray; CT scan
caries cellulitis and edema of the Surgical Management:
Chronic - slowly progressive, a adjacent facial structures
fully formed abscess may occur and mobility of the
Invasion of pathogens: - Incision and Drainage
bacteria -Administer antibiotics as
without the patient’s knowledge, involved tooth prescribed by the physician
leads to a “blind dental abscess” • difficult to open the mouth -Give analgesics as prescribed
w/c is a periapical granuloma, • fever
discovered on X-ray, treated w/ Activation and release of Nursing Management:
• Malaise -Assess for bleeding after
root canal therapy Cytokines
• Affected teeth loosen treatment and is instruct to use
• Fistula formation to drain a warm saline or warm water
the abscess mouth rinse to keep the area
clean.
Stimulation of immune cells -Take antibiotic and analgesic
and dilation of capillaries agents as prescribed
- Advance from a liquid diet to a
soft diet as tolerated
-Keep follow-up appointments
Formation of pus(immune
response)

Abscess Formation
Malocclusion
-Misalignment of the teeth of the upper and lower dental arcs when the jaws are closed
-most common developmental oral problem

- Inherited or acquired CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

- Makes the teeth difficult to
clean and can lead to decay, -teeth that are crooked ; Diagnostics: X-ray
crowded, widely spaced or stick Genetics -Begins when the patient has
gum disease Tooth loss
out shed the last primary tooth and
-speech problems Prolonged use of pacifier the last permanent successor
-change in facial structures Thumb sucking has erupted
-frequent biting of tongue and Cleft lip and palate Surgical Management
cheeks Injuries and trauma -Corrections requires an
Tumors in the mouth orthodontist
Bottle feeding -orthodontist gradually forces
Impacted tooth the teeth into a new location by
Lack of oral care using wires or plastic bands
Airway obstructed by enlarged
(braces)
adenoids or allergies
-final phase of treatment:
retaining device is worn for
several hours each day to
Disruption in the normal support the tissues as they
growth of teeth adjust to the new alignment of
the teeth.
Nursing Intervention:
-Meticulous oral care
Misaligned teeth -Assess psychological impact of
having wires and braces
 Bacterial Parotitis -inflammation of the parotid gland
- may be due to mumps (epidemic parotitis)
• most common inflammatory CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
condition of the salivary glands
• elderly, acutely ill, debilitated • onset is sudden, • adequate nutritional and fluid
• Fever
• older, acutely intake, good oral hygiene, and
people with decreased salivary
flow from dehydration or • gland swells and becomes • debilitated with discontinuing medications (e.g.,
medications are at higher risk tense and tender decreased salivary tranquilizers, diuretic agents) that
• usually caused by • Pain • flow from general can diminish salivation
Staphylococcus aureus • Difficult swallowing • Antibiotic therapy is necessary
dehydration for bacterial parotitis
• medications • Analgesics may be prescribed to
control pain
Surgical Management
Break in the integrity of oral • Parotidectomy: if antibiotic
mucosa therapy is not effective

Invasion of S. aureus into the

parotid duct

Parotitis
MUMPS
- epidemic parotitis, a communicable disease caused by a viral infection mostly affect children
-acute systemic viral infection usually associated with pain and swelling of the salivary glands
-an illness characterized by acute-onset unilateral or bilateral tender, self-limited swelling of the parotid or other
salivary gland(s) that lasts at least 2 days and has no other apparent cause.
-Agent: Paramyxovirus
Incubation period: 14 to 21 days CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Communicable period: Immediately
• Fever • Institute airborne droplet
before and after parotid gland
swelling begins • Headache and malaise precautions.
Source: Saliva of infected person • Anorexia • Provide bedrest until the parotid
• Jaw or ear pain aggravated by gland swelling subsides.
and possibly urine
chewing, followed by parotid • Avoid foods that require chewing.
Transmission: Direct contact or
glandular swelling • Apply hot or cold compresses as
droplet spread from an infected
• Orchitis may occur prescribed to the neck.
person
• Give antipyretics, pain meds
• Adequate hydration.
• Apply warmth and local support
with snug fitting underpants to
relieve orchitis.
 SIALADENITIS -inflammation of the salivary gland
-Agent: Staphylococcus aureus; Streptococcus viridans
- In hospitalized or institutionalized patients, the infecting organism may be methicillin-resistant S. aureus (MRSA)

• caused by dehydration, radiation CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

therapy, stress, malnutrition,
salivary gland calculi, improper • Pain while eating • antibiotics
• Salivary stone or a kink
oral hygiene • Swelling • massage
• may be induced by trauma, viral • Purulent discharge or blockage in the duct • hydration
or bacterial infection, or • Fever of the gland • warm compresses
autoimmune disease • Decreased saliva (a symptom • Inadequate fluid • sialagogues
• most prevalent form of of both acute and chronic consumption, illness, or • corticosteroids
sialadenitis is the mucocele. sialadenitis) medications such as Surgical Management:
• most common viral cause of • Dry mouth (xerostomia) diuretics (water pills) or Surgical drainage or excision of the
sialadenitis is mumps, which • Reddened skin antihistamines gland and its duct are considered in
affects the major salivary glands, • Swelling in the cheek and neck • Sjogren syndrome cases of sialadenitis that are
particularly the parotids region recurrent or refractory to antibiotics.

* Chronic sialadenitis is typically due Dryness of mouth

to decreased salivary flow.

Break in the mucosa of

salivary glands

Invasion of bacteria or
viruses

Sialadenitis
MUCOCELE
 SALIVARY CALCULUS -’’salivary stones”
-condition in which the precipitation of salts in the saliva forms a stone effectively blocking the flow of saliva from the gland to
(SIALOLITHIASIS) the oral cavity

usually occur (in 80% to 90% of CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

cases) in the submandibular gland
formed mainly from calcium • gland is swollen, Exact mechanism: Not Clear • Antibiotics
phosphate • tender, palpable w/ stone • Hydration
• Fever and chills Accumulation of mucus, bacteria, • warm compresses
desquamated epithelial cells, • massage
dehydration, trauma • Extraction, lithotripsy
• Surgery may be necessary to
Formation of Nidus remove the gland if symptoms
and calculi recur repeatedly.

Retention of Nidus in the ductal

lumen

Nidus provides an environment

for attachment and deposition
of salivary minerals

Formation of sialolith
Can occur in 3 major salivary glands
(parotid, submandibular, sublingual).
Blockage of salivary gland
Associated with salivary stasis (eg,
dehydration) and trauma inflammation leading to
Sialolithiasis
DISORDERS OF THE JAW
 Temporomandibular -Aka temporomandibular joint syndrome, represent an array of pathologies affecting the TMJ and its surrounding
structures
Disorders
categorized as follows (National CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Institute of Dental and Craniofacial
Research): • Jaw pain ; dull ache to throbbing, Diagnostics: Clinical/ based on
debilitating; pain that can radiate Congenital malformation, history/S/sx
Myofascial pain—a discomfort in the to the ears, teeth, neck muscles, fracture, chronic dislocation, MRI: only used for severe or
muscles controlling jaw function and and facial sinuses cancer, and syndromes chronic symptoms
in neck and shoulder muscles • restricted jaw motion and
locking of the jaw Nursing Management:
Internal derangement of the joint—a • sudden change in the way the combination of simple noninvasive
dislocated jaw, a displaced disc, or upper and lower teeth fit therapies that :
an injured condyle • clicking, popping, and grating INTRA-ARTCULAR • Patient education on self-care
MUSCLES
sounds when the mouth is JOINTS • Cognitive behavioral therapy,
Degenerative joint disease— opened, and chewing and • Physical therapy, exercise and
rheumatoid arthritis or osteoarthritis swallowing manual therapy
in the jaw joint • Headaches • analgesics (NSAIDs] and muscle
• Earaches relaxants initially) as prescribed
• Dizziness • oral appliance therapy
• Hearing problems • A liquid or soft diet may be
primarily affects women with a male- recommended for up to 4 to 6
to-female ratio of 1:4. weeks; after “wiring the jaw shut”
• Dietary counseling should be
obtained to ensure optimal
caloric and protein intake
ESOPHAGEAL DISORDERS
 Hiatal Hernia
-opening in the diaphragm through w/c the esophagus passes becomes enlarged and part of the upper stomach
tends to move up
-also known as esophageal or diaphragmatic hernia
-the most common abnormality found on x-ray examination of the upper GI tract
More common among women CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Two types:
• Heartburn Diagnostics: BARIUM SWALLOW
-A. Sliding or type I hiatal hernia
• Regurgitation Nursing Interventions:
(most common- 90%)
• Dysphagia 1. Provide small frequent feedings
-B. Paraesophageal hiatal hernia :
• Foul breath 2. AVOID supine position for 1 hour
type II, III and IV ( IV- greatest
• 50%- without symptoms after eating
herniation)
3. Elevate the head of the bed on 8-
inch block
4. Provide pre-op and post-op care

Type 1: treated medically with

antacids, small meals, elevation
of head after meals; 15% of
HIATAL HERNIA
cases may require surgery:
Nissen Fundoplication.
Complications :
• Ulceration
• Hemorrhage, Type 2- 4: Elective Surgery
• Regurgitation and aspiration of because of the complication
stomach contents
• Strangulation
• Incarceration of the
• Stomach in the chest with possible
necrosis
• Peritonitis
• Mediastinitis
 Achalasia
-absent or ineffective peristalsis of the distal esophagus accompanied by failure of the esophageal sphincter to
relax in response to swallowing which leads to narrowing of esophagus and gradual dilation in the upper chest
-Failure of LES to relax due to degeneration of inhibitory neurons (containing NO and VIP) in the myenteric
(Auerbach) plexus of esophageal wall.
may progress slowly and occurs CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
most often in people 40 years
• Main symptom : Diagnostics:
or older. • X-ray studies show esophageal
dysphagia
• Non-cardiac chest or dilation above the narrowing at
epigastric pain the gastroesophageal junction.
• Barium swallow
• Pyrosis: heartburn
• Computed tomography (CT)
• Regurgitation • scan of the chest
• Weight loss • Endoscopy may be used for
• Recurrent pulmonary diagnosis
Complications • Manometry
Nursing Management
• Instruct patient to eat slowly and
to drink fluids with meals
• Give oral calcium channel
blockers and nitrates as
prescribed
• Injection of botulinum toxin
(Botox) into quadrants of the
esophagus via endoscopy
• Pneumatic dilation
Surgical Managemrnt
Heller Myotomy: circular muscle
layer of LES is incised.
 Esophageal Dilation and tortuosity of the submucosal veins in the distal esophagus
- ETIOLOGY: commonly caused by PORTAL hypertension secondary to liver cirrhosis

Varices
Emergency condition! CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Complication: RUPTURED • Hematemesis DIAGNOSTIC PROCEDURE :
VARICES • Melena Esophagoscopy
Rupture and resultant hemorrhage • Ascites - NURSING INTERVENTIONS:
• Jaundice 1. Monitor VS strictly. Note for signs of
of the esophageal varices is the
• Hepatomegaly/splenomegaly shock
primary concern because it is a life- 2. Monitor for LOC
threatening situation 3. Maintain NPO
SIGNS OF SHOCK 4. Monitor blood studies
• tachycardia 5. Administer O2
• Hypotension 6. Prepare for blood transfusion
• Tachypnea 7. Prepare to administer Vasopressin
• cold clammy skin and Nitroglycerin
• narrowed pulse pressure 8. Assist in NGT and Sengstaken-
Blakemore tube insertion for balloon
tamponade
9. Prepare to assist in surgical
management:
   Endoscopic sclerotherapy
   Variceal ligation
   Shunt procedures
Sengstaken-
Blakemore
Tube
 Shunting
procedures
 ESOPHAGEAL -out-pouching of mucosa and submucosa that protrudes through a weak portion of the musculature of
the esophagus.
DIVERTICULUM -may occur in one of the three areas of the esophagus— pharyngoesophageal (upper), midesophageal
(middle), or epiphrenic (lower).
-AKA pharyngoesophageal diverticulum, pharyngeal pouch, hypopharyngeal diverticulum
• Most common type: Zenker CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
diverticulum • Dysphagia Diagnostics:
(pharyngoesophageal) Esophageal dysmotility • Barium swallow
• Fullness in the neck, Belching
• usually seen in people older • Regurgitation of undigested • Manometric studies
than 60 years of age food Esophagoscopy: contraindicated
• Most common in elderly Uncoordinated swallowing, because of the danger of perforation
• Gurgling noises after eating impaired relaxation and
males. of the diverticulum
• Halitosis swallowing, impaired Surgical Management
• Sour taste in the mouth relaxation and spasm of Diverticulectomy: only means of
cricopharyngeus muscle cure is surgical removal of the
diverticulum.
Myotomy of the cricopharyngeal
Increased pressures in distal muscle
pharynx Surgery is indicated for epiphrenic
and midesophageal diverticula only
if the symptoms are troublesome
Excessive lower pharyngeal and becoming worse.
pressures Nursing Management:
• If regurgitating: elevate pt.
head;turned to one side
Herniation of mucosal tissue • Administer ordered antacids and
provide antireflux care.
• Regularly assess the patient’s
nutritional status.
Diverticulum formation • Monitor respiratory s/sx that
suggest aspiration
 Gastro-esophageal reflux - Backflow of gastric contents into the esophagus
Disease (GERD) - Usually due to incompetent lower esophageal sphincter , pyloric stenosis or motility disorder
- Most common upper GI problem
-Symptoms may mimic ANGINA or MI CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
- Incidence increases w/ aging
Classification: • Heartburn / Pyrosis Diagnostic test
Physiologic (or functional) • Dyspepsia / Indigestion -Endoscopy or barium swallow
gastroesophageal reflux. These • Regurgitation - Gastric ambulatory pH analysis
patients have no underlying • Odynophagia *Note for the pH of the esophagus,
predisposing factors or conditions; • Dysphagia / Difficulty swallowing usually done for 24 hours
growth and development are normal, • Excessive salivation *The pH probe is located 5 inches
and pharmacologic treatment is above the lower esophageal sphincter
typically not necessary. *The machine registers the different pH
Pathologic gastroesophageal reflux of the refluxed material into the
or gastroesophageal reflux disease esophagus
(GERD). Patients frequently experience Nursing Interventions:
some complications, requiring 1. Instruct the patient to AVOID stimulus
careful evaluation and treatment. that increases stomach pressure and
Secondary gastroesophageal reflux. decreases LES pressure
- refers to a case in which an underlying 2. Instruct to avoid spices, coffee,
condition may predispose to tobacco and carbonated drinks
gastroesophageal reflux; examples 3. Instruct to eat LOW-FAT, HIGH-
include asthma (a condition which may FIBER diet
also be, in part, caused by or 4. Avoid foods and drinks TWO hours
exacerbated by reflux) and gastric before bedtime 5.Elevate the head of
outlet obstruction. the bed with an approximately 8-inch
block
6. Administer prescribed H2-blockers,
PPI and prokinetic meds like Cisapride,
Metoclopromide
7. Advise proper weight reduction
 -Inflammation of the stomach or gastric mucosa
Gastritis
May be Acute or Chronic CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
- Etiology:
Acute - irritating foods, highly seasoned Diagnostic Procedure
ACUTE
or contaminated with disease causing EGD- to visualize the gastric mucosa
microorganism, NSAIDS, alcohol, bile Abdominal discomfort for inflammation
reflux and radiation treatment Anorexia, nausea, and • Absent (Achlorhydria) or Low levels
Chronic- Ulceration, bacteria vomiting of HCl (hypochlorhydria) or High
(Helicobacter pylori), Autoimmune Headache Levels of HCl (hyperchlorhydria)
disease (pernicious anemia), diet Hiccupping BIOPSY to establish correct diagnosis
(caffeine), alcohol, smoking, bile reflux whether acute or chronic

CHRONIC NURSING INTERVENTIONS:

• Give BLAND diet
Anorexia, nausea, and • Monitor for signs of complications
vomiting like bleeding, obstruction and
Belching pernicious anemia
Heartburn after eating • Instruct to avoid spicy foods,
Sour taste in the mouth irritating foods, alcohol and caffeine,
Vitamin B12 deficiency NSAIDS,
• Administer prescribed medications-
H2 blockers, antibiotics, mucosal
protectants
• Inform the need for Vitamin B12
injection if deficiency is present
 - an ulceration in the mucosal wall of the stomach, pylorus, duodenum, or esophagus in portions accessible to gastric secretions;
Peptic Ulcer erosion may extend through the muscle
Disease - most common peptic ulcers are gastric ulcers and duodenal ulcers

CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

GASTRIC Pharmacologic therapy- combination

• Gnawing, sharp pain in of antibiotics, proton pump inhibitors
or left of the mid- and bismuth salt to eradicate H.pylori
epigastric region for 10-14 days, Histamine-2 (H2)
occurs 30 to 60 receptor antagonist and PPI are used
minutes after a meal to treat NSAID induced ulcers
(food ingestion Surgical Management
accentuates the pain). Total gastrectomy
• Hematemesis is more • Vagotomy
common than melena. • gastric resection
Most common Peptic ulceration: DUODENAL • Billroth I and II
anterior part of the upper • Burning pain occurs in • Pyloroplasty
duodenum the mid-epigastric area Nursing Interventions:
1  to 3 hours after a 1. Give BLAND diet, small frequent
- Common between 40-60 y/o, meal and during the meals during the active phase of the
blood type O; blood type A disease
night (often awakens
- Causes: H.pylori infection, 2. Administer prescribed medications-
excessive secretion of HCl, the client). H2 blockers, PPI, mucosal barrier
stress, alcohol, smoking, • Melena is more protectants and
caffeinated beverage, spicy foods common than antacids
hematemesis. 3. Monitor for complications of bleeding,
• Pain is often relieved perforation and intractable pain
by the ingestion of 4. Provide teaching about stress
food. reduction and relaxation techniques
Zollinger-Ellison Syndrome- severe Stress ulcer - occurs after physiological
peptic ulcer, extreme gastric hyperacidity, stressful events such as burns, shock,
and gastrin secreting benign or malignant sepsis, trauma, ventilator-assisted patient, Complications of Peptic Ulcer
tumors of the pancreas-resistant to
standard medical treatment
Disease

Cushing’s ulcer - common in pts w/ head Curling’s ulcer – Proximal duodenal ulcers
injury and brain trauma, more penetrating associated with severe burns and trauma
and deeper than stress ulcer, involves -observed about 72 hours after extensive
esophagus, stomach and duodenum burns
-Aka von Rokitansky–Cushing syndrome
PHARMACOLOGY
Histamine-2 (H2) receptor antagonists Proton Pump Inhibitor
(PO/IV)
Action: Action:
• Reversible block of histamine H2- • Irreversibly inhibit H+/K+
receptors→ ↓ H+ secretion by parietal ATPase in stomach parietal
cells. cells
• Prevents the release of gastrin, a • bind to the H+/K+-ATPase
hormone that causes local release of enzyme system (proton
histamine (due to stimulation of histamine pump) and suppress the
receptors), ultimately blocking the secretion of hydrogen ions
production of hydrochloric acid. into the gastric lumen
• Taken with meals or at H.S. • 4-8 weeks medications
• Cigarettes reduces its action • Esomeprazole (Nexium)
• SE: headache, dizziness, nausea/vomiting • Omeprazole (Prilosec)
& urticaria • Lansoprazole (Prevacid)
• 8 weeks medication (if s/sx does not • Pantoprazole (Protonix)
improve, start antibiotics)
• Cimetidine (Tagamet): confusion
• Ranitidine (Zantac)
• Famotidine (Pepcid)
• Nizatidine (Axid) Adverse effects of proton
pump therapy.
PHARMACOLOGY

Antibiotics Antacids (non absorbable)

• Action: antibacterial to eradicate H. • Action: ↓ gastric acidity

pylori • Chew then swallow, taken 1 hr after meals
• Amoxicillin (Amoxil) or at H.S.
• Clarithromycin (Biaxin) Aluminum Hydroxide :
• Metronidazole (Flagyl) • Don’t give other drugs w/in 1-2 hrs after the
• Tetracycline antacids
• Can be combined with other drugs Magnesium Oxide
• Taken in between meals or at bedtime
• May increase serum Magnesium level in
RF client
• Chew follow with water
Calcium Carbonate
• Taken in between meals or at bedtime with
milk
NaHCO3
PHARMACOLOGY
Mucosal Barrier
Also known as cytoprotective compounds

Action:
• forms protective barrier, adheres to ulcer surface
• Bind to ulcer base, providing physical protection and
allowing HCO3– secretion to reestablish pH gradient
in the mucous layer
• 30 min interval before taking antacids
• SE: constipation, and nausea/vomiting
• Give 1-2 hour after meal or during bedtime on an
empty stomach
• 5 hours duration
• Sucralfate (Carafate): requires acidic environment, not
given with PPIs/H2 blockers.
Surgical Procedures NURSING INTERVENTIONS FOR
BLEEDING
Vagotomy : severing of the Billroth I – Gastroduodenostomy Billroth II – Gastrojejunostomy 1. Maintain on NPO
vagus nerve • Removal of the lower portion of the • Remaining portion is anastomosed to 2. Administer IVF and medications
• Decreases gastric acid antrum the jejunum 3. Monitor hydration status, haematocrit
• Diminishing cholinergic • Antrum contains the cells that secretes Dumping syndrome and hemoglobin
stimulation to the parietal gastrin  Anemia 4. Assist with SALINE lavage
cells- less responsive to • Small portion of duodenum and pylorus  Malabsorption 5. Insert NGT for decompression and
gastrin • Remaining portion is anastomosed to the  Weight loss lavage
duodenum  Recurrence rate of ulcer is 10-15% 6. Prepare to administer blood transfusion
 Feeling of fullness 7. Prepare to give VASOPRESSIN to
 Dumping syndrome induce vasoconstriction to reduce
 Diarrhea bleeding
 Recurrence rate is <1% 8. Prepare patient for SURGERY if
warranted

Post-operative Nursing management

1. Monitor VS
2. Post-op position: FOWLER’S
3. NPO until peristalsis returns
4.Monitor for bowel sounds
5. Monitor for complications of surgery
6.Monitor I and O, IVF
7. Maintain NGT
8. Diet progress: clear liquid    full liquid
   six bland meals
9. Manage DUMPING SYNDROME
DUMPING SYNDROME Aka: Rapid gastric emptying; Vagotomy syndrome
A condition of rapid emptying of the gastric contents into the small intestine
usually
after a gastric surgery. Symptoms occur 30 minutes after eating
PATHOPHYSIOLOGY MANAGEMENT
Post gastric surgery
1. Advise patient to eat LOW-
carbohydrate, HIGH-fat and
HIGH-protein diet
2. Instruct to eat SMALL
frequent meals, include
MORE dry items.
3. Instruct to AVOID
consuming FLUIDS with
meals
4. Instruct to LIE DOWN after
meals
5. Administer anti-spasmodic
medications to delay gastric
emptying
 cancer is a malignant growth of the mucosal cells in the inner lining of the stomach, with invasion to the
Gastric Cancer muscle and beyond in advanced disease
-5th most common cancer diagnosis
40-70 y/o, more common among CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
men
mean age at diagnosis : 69 years Asymptomatic in the early stage Diagnostics
EARLY SYMPTOMS OF GASTRIC
CANCER • History and •• CBC; Liver
- Diet high in smoke foods, low in a. Indigestion physical enzymes
fruits and vegetables b. Abdominal discomfort examination • Urinalysis
- Chronic inflammation of the • Endoscopy and • Stool examination
c. Full feeling biopsy • Serum amylase
stomach d. Epigastric, back, or retrosternal pain • CT, MRI, PET scans • Tumor markers
- Pernicious anemia • Upper GI barium • α-Fetoprotein
- Obesity LATE SYMPTOMS OF GASTRIC study • Carbohydrate
- Gastric ulcers CANCER • Exfoliative cytologic antigen (CA)-19-9,
a. Weakness and fatigue study CA-125, CA 72-4
- H. Pylori infections • Endoscopic • Carcinoembryonic
b. Anorexia and weight loss
- Chronic Smoking ultrasonography antigen (CEA)
c. Nausea and vomiting
- Previous Subtotal Gastrectomy d. A sensation of pressure in the
- Genetics stomach Nursing Management
prognosis :generally POOR e. Dysphagia and obstructive symptoms • Monitor vital signs.
f. Iron deficiency anemia
5- year survival rate : 29% g. Ascites
• Monitor Hgb and Hct and administer blood
transfusions as prescribed.
h. Palpable epigastric mass • Monitor weight.
Advanced Gastric cancer- • Assess nutritional status; encourage
palpable mass small, bland, easily digestible meals with
- Ascites and Hepatomegaly- if vitamin and mineral supplements.
cancer cells metastasized to the • Administer pain medication as prescribed.
• Prepare the client for chemotherapy or
liver radiation therapy as prescribed.
- Sister Mary Joseph’s Nodule- • Prepare the client for surgical resection of
palpable nodules around the the tumor as prescribed
umbilicus
 LOWER
GASTROINTESTI
NAL TRACT
DISORDERS
FLORENCE IVAN C. TUBBAN, RN
 h e

ice nuts (hard to onc4

1.bh,xeIffomd boel moerenb. out 1umpy

2. Eait pass@xih0pgin. Line a aucage aux wizN

Like a sausage or snake.

4. A6leooztolfmvqeoalleéetopetat ilet mooth to soft

6. ¥oidarnpIe\in nesting.
rlwffy pieces with ragged

Iam.b&pteâ6mC04yrl/e&uuIationdAuAalb@16).
&otYourB0¥el.RdriP/ed6n <¥nu.«4ner¥e.oqadpages/
 Constipation
- Abnormal hardening of stools
- Irregularity of elimination
- Retention of stool for a prolonged period

3 classes of constipation, based CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

upon their underlying
pathophysiologic mechanisms • Abdominal distention Diagnostics
• Inadequate fiber or fluid intake
• Borborygmus • Patient’s history
and/or Overuse of caffeine or
Functional constipation • gurgling sound caused by alcohol • physical examination, possibly
• most common passage of gas in the • Medication the results of a barium enema
• can be successfully treated by intestine • Systemic endocrine or or
increasing intake of fiber and • Pain and pressure neurologic diseases • Sigmoidoscopy
fluids • Indigestion • Psychological issues (stressful) • stool testing for occult blood
• Sensation of • Intestinal conditions • Anorectal manometry
Slow-transit constipation
incomplete emptying • Neoplasms • Defecography and colonic
• caused by inherent disorders of
the motor function of the colon • Straining transit studies
• characterized by infrequent • Hard, dry stools • pelvic floor magnetic
bowel movements Impaired anorectal function resonance imaging (MRI)
Defecatory disorders
• caused by dysfunctional motor Nursing Management
coordination between the pelvic • Providing patient education
Reduced frequency or absence of • Bowel habit training
floor and anal sphincter peristaltic contractions
• Increased fiber and fluid intake
• Discontinue laxative abuse
• Biofeedback
Constipation • Exercise to strengthening
abdominal muscles
 -- Increased frequency of bowel movement more than 3x a day

Diarrhea - Increased amount of stool

- Altered consistency

can be classified as: CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT

• Acute diarrhea is self-limiting, • Abdominal Diagnostic :
lasting 1 or 2 days cramps, Distention Acute and Chronic diarrhea: - CBC count
• Persistent diarrhea typically • Intestinal rumbling/ Persistent diarrheas • Secretory
- Chemical profile
lasts between 2 and 4 weeks noninflammatory • Osmotic
borborygmus - Urinalysis
• Chronic diarrhea persists for (large-volume) or Malabsorptive
• Anorexia and thirst inflammatory (small- • Infectious - Stool exam
more than 4 weeks and may • Painful spasmodic - Endoscopy or barium enema
volume) • Exudative
return sporadically contractions of Nursing Management
C. difficile is the most commonly the anus • Monitor vital signs.
identified agent in antibiotic- • Tenesmus Invasion the • Assess the characteristics and
associated diarrhea in the hospital intestinal mucosa
pattern of diarrhea.
MOST COMMON COMPLICATION
• Inspection of the abdomen,
of diarrhea is : dehydration ↑intestinal
Inflammation secretions mucous membranes, and skin
↓mucosal • Patient is encouraged to increase
absorption • intake of liquids and foods low in
bulk until the symptoms subside
• Patient should avoid caffeine,
Altered Motility alcoholic beverages, dairy
products, and fatty foods for
Diarrhea several days
• Antidiarrheal medications such as
diphenoxylate with atropine or
loperamide may be taken as
prescribed
• Intravenous (IV) fluid therapy may
be necessary for rapid rehydration
• Monitor serum electrolyte levels
closely.
 -recurrent involuntary passage of stool from the rectum for at least 3 months.
Fecal Incontinence -Inability of the rectum to sense and accommodate stool
-aka as Encopresis
Factors that influence this disorder: CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
• Ability of the rectum to sense • Soiling Diagnostics
and accommodate stool
• Occasional urgency • After rectal surgeries • Rectal examination Flexible
• Amount and consistency of
and loss of control • Scleroderma sigmoidoscopy
stool
• Complete incontinence • Neuropathies • Anorectal
• Integrity of the anal sphincters
• Poor control of flatus • Disorders of the pelvic floor • Manometry
and
• Diarrhea • Inflammatory disorders (intestinal) • Anal endosonography
• Musculature
• Constipation • CNS disorders • Pelvic MRI scan
• Rectal motility
• Diarrhea • Transit studies
• Fecal impaction with overflow Nursing Management
• Behavioral disorders • Identify frequency, volume,
and consistency of the feces
• Administering loperamide 30
minutes prior to meals as
Disrupt the structure or function of
prescribed
the anorectal unit
• Maintaining skin integrity is a
priority
Impaired reflex relaxation of anal • Assist the patient and family to
sphincter accept and cope with this
chronic situation.
• Biofeedback therapy
Fecal Incontinence • Bowel training programs
Surgical Management
• Sacral nerve stimulation
• Surgical reconstruction,
sphincter repair or fecal
diversion
 Irritable bowel -chronic functional disorder (no structural abnormalities) characterized by recurrent abdominal pain associated with
disordered bowel movements, which may include diarrhea, constipation, or both
syndrome (IBS)
- peak prevalence of IBS is CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
between 20 and 40 years
• main symptom: alteration in Diagnostics
- Middle Aged Women > Men are genetic, environmental, and
bowel patterns: • Bristol Stool Form Scale
affected psychosocial factors
constipation (IBS-C) • CBC and C-reactive protein
diarrhea (IBS-D) or fecal calprotectin can rule
Precipitated by
combination (IBS-M out IBD
Recurrent abdominal pain
“mixed”) unknown (IBS-U) • Stool studies Colonoscopy
associated with ≥ 2 of the following: • chronic stress,
• relapsing abdominal Nursing Management
• Related to defecation • sleep deprivation
pain, bloating and • Goals of treatment are to relieve
• Change in stool frequency • surgery
distention abdominal pain and control
•   Change in form • infections
diarrhea or constipation
(consistency) of stool • diverticulitis
• some foods (milk, yeast • First-line treatment is lifestyle
clinical manifestations of IBS must products, eggs, wheat modification and dietary changes
be present sometime during the last products, red meat) • IBS-D: give anti-diarrheal agents
3 months with onset for at least 6 as prescribed
months prior to diagnosis • Provide patient and family
• GI motor disturbances education and encourage self-
• Enteric Neuropathy care activities
• Visceral Hypersensitivity • Nurse emphasizes and
• Abnormal central processing of reinforces good sleep habits and
Sensations good dietary habits
• Alcohol use and cigarette
Alteration in bowel patterns smoking are discouraged.
• Stress management via
relaxation techniques, cognitive-
IBS behavioral therapy, yoga, and
exercise can be recommended
● ACUTE ABDOMEN: also known as surgical abdomen
● Characterized by an acute onset of abdominal pain that does not have a
traumatic etiology
● most typically requires swift surgical intervention to prevent peritonitis, sepsis,
and septic shock
● include appendicitis, severe diverticulitis, and intestinal obstruction
 Appendicitis -Inflammation of the vermiform appendix
-most common reason for emergency abdominal surgery.
• can occur at any age CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
• typically occurs between the
ages of 10 and 30 years • Abdominal pain: begins in the Diagnostics
• Fecalith
• -incidence is slightly higher umbilicus then localizes in the • CBC- reveals increased WBC count
• lymphoid
among males RLQ (Mc Burney’s point) • hyperplasia (secondary to • Ultrasound
• there is a familial predisposition • Anorexia inflammation or infection) • Abdominal X-ray
• Nausea and Vomiting • rarely, foreign Surgical Management:
Etiology: usually fecalith, lymphoid • Fever • bodies (fruit seeds) or - Appendectomy
hyperplasia, foreign body and • Rebound tenderness and tumors Nursing Management
helminthic obstruction abdominal rigidity (if - Preoperative care
perforated) Obstruction of appendix - NPO
• Constipation or diarrhea - Consent
- Monitor for perforation and signs of shock
Distention; ↑ intraluminal - Monitor bowel sounds, fever and hydration
pressure status
- POSITION of Comfort: RIGHT SIDELYING
in a low Fowler’s
Edema - AVOID laxatives, enemas and HEAT
APPLICATION
- SURGERY: APPENDECTOMY
Ischemia - Post operative Care:
- Monitor VS and signs of
surgical complications
Bacterial Overgrowth - Maintain NPO until bowel function returns
Psoas Sign Obturator Sign - If rupture occurred, expect drains and IV
Gangrene antibiotics
- POST OP. POSITION: RIGHT SIDE-LYING,
SEMI-Fowler’s to decrease tension or incision
Perforation and legs flexed to promote drainage

Appendicitis
 Peritonitis
-inflammation of the peritoneum
-a result of bacterial infection but may occur secondary to a fungal or mycobacterial infection
-most common bacteria implicated are Escherichia coli and Klebsiella, Proteus, Pseudomonas, and
Streptococcus species.
Can be categorized as: CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
Primary peritonitis:
• Fever, chill, tachycardia Diagnostics
• also called spontaneous • inflammation • CBC
• Pain is diffuse but then becomes
bacterial peritonitis (SBP) • Infection • Serum electrolyte studies
constant, localized, and more
• occurs as a spontaneous • ischemia • Abdominal x-ray
intense over the site of the
bacterial infection of ascitic • trauma • computed tomography (CT) scan
pathologic process
fluid • tumor perforation • Peritoneal aspiration and culture and
• Movement usually aggravates
• most commonly in adult • sensitivity studies
pain
patients with liver failure Nursing Management
• Abdomen becomes extremely
Secondary peritonitis Fluid, colloid, and electrolyte replacement
tender and distended, and the
• occurs secondary to perforation leakage of contents from is the major focus of medical
muscles
of abdominal organs with abdominal organs into the
• become rigid (board-like) management.
spillage that infects the serous abdominal cavity • Administration of several liters of an
• Rebound tenderness
peritoneum isotonic solution as prescribed
• anorexia,
• most common causes include a Bacterial growth/ proliferation • Administer analgesics, antiemetic
• nausea, and vomiting
perforated appendix ,perforated agents as prescribed
• Paralytic ileus
peptic ulcer , perforated sigmoid • Intestinal intubation and suction
colon caused by severe • Signs of shock • Oxygen therapy by nasal cannula
Edema of the tissues
diverticulitis , volvulus of the or mask
colon , and strangulation of the Signs indicating that peritonitis is • Administer IV antibiotics as prescribed
small intestine. subsiding : Exudation of fluid in the main focus of treatment in secondary
Tertiary peritonitis • ↓ temperature ,PR peritoneum peritonitis is to identify the source of
• occurs as a result of a supra- • Softening of the abdomen infection and eradicate it.
infection in a patient who is • Return of peristaltic sounds, • Surgical treatment is directed toward
Passing of flatus, Peritonitis excision , resection with or without
immunocompromised.
• Presence of bowel movements anastomosis , repair ,and drainage.
• Tuberculous peritonitis in a • With extensive sepsis, a fecal diversion
patient with AIDS
 DIVERTICULOSIS AND -Diverticulosis
DIVERTICULITIS Abnormal out-pouching of the intestinal mucosa occurring in any part of the LI most commonly in the sigmoid
Diverticulitis
Inflammation of the diverticulosis
Diverticular Disease CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
- Diverticulum: sac-like herniations DIAGNOSTICS
• Left lower Aging
of the lining of the bowel that extend fiber- Hardened 1.If no active inflammation,
Quadrant pain
through a defect in the muscle layer deficient fecal COLONOSCOPY and Barium Enema
• Flatulence
-May occur anywhere in the Straining during contents masses
• Bleeding per rectum 2.CT scan is the procedure of choice!
intestine, but are most common in defecation
• nausea and vomiting 3.Abdominal X-ray
the sigmoid colon NURSING INTERVENTIONS:
• Fever high low ↓ muscle
-Diverticulosis: multiple diverticula • Maintain NPO during acute phase
• Palpable, tender intraluminal volume strength in
without inflammation • Provide bed rest
rectal mass pressure in the the colon
-Diverticulitis: infection and • Administer antibiotics, analgesics
colon wall
inflammation of diverticula like meperidine (morphine is not
-Diverticular disease increases used) and anti-spasmodics
with age and is associated with a ↓tensile strength • Monitor for potential
low-fiber diet and elasticity complications like perforation,
hemorrhage and fistula
• Increase fluid intake
• Avoid gas-forming foods or HIGH-
mucosal and submucosal layers of the roughage foods containing seeds,
colon herniate through the muscular wall nuts to avoid trapping
• Introduce soft, high fiber foods
Diverticulum formation ONLY after the inflammation
subsides
Accumulation of bowel contents in the diverticulum
• Instruct to avoid activities that
increase intra-abdominal pressure

Inflammation → Infection

Diverticulitis
Hinchey Classification: Staging of Acute, Complicated Diverticulitis
 Intestinal Obstruction
Mechanical Obstruction Neurogenic
Intraluminal obstruction or mural obstruction from pressure on the intestinal -Paralytic ileus
wall occurs -Adynamic ileus
□ Stenosis, adhesions, hernias
Vascular
Functional obstruction -Occlusion of arterial blood supply
The intestinal musculature cannot propel the contents along the bowel -Mesenteric thrombosis
□ Muscular dystrophy, endocrine disorders or neurologic disorders -Abdominal angina
-Small Bowel Obstruction
Mechanical: -Intestinal contents, fluids and gas accumulate above the intestinal obstruction
-Adhesions – fibrous band of scar tissue from surgery -Reduce the absorption of fluids and stimulate more gastric secretion
-Hernias – incarcerated or strangulated -Pressure within the intestinal lumen increases
-Volvulus – twisting of bowel -Decrease in venous and arteriolar capillary pressure
-Intussusception – telescoping of the bowel upon itself -Edema, congestion, necrosis, and rupture or perforation of intestinal wall → peritonitis
-Tumors -Reflux vomiting leads to ↓K+, ↓Clˉ in blood, with fluid losses resulting to shock
-Hematoma
-Fecal impaction
-Intraluminal obstruction
-Intussusception
-Volvulus
 Small Bowel -Accumulation of intestinal contents, fluid, and gas proximal to the obstruction

Obstruction
Most bowel obstructions occur in CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
the
small intestine.
• Initial symptom : usually crampy Adhesions Diagnostics:
Adhesions are the most common pain that is wavelike and colicky Tumors • Abdominal x-ray and CT scan
due to persistent peristalsis findings
cause of small bowel obstruction, Crohn’s • Laboratory studies (i.e., electrolyte
followed by tumors, Crohn’s • pass blood and mucus but no disease
fecal matter and no flatus studies and a CBC) approach to
disease, and hernias Hernias small bowel obstruction focuses:
• Vomiting occurs.
(1) confirming the diagnosis
Signs of dehydration become (2) identifying the etiology
evident: Intestinal contents, fluid,
(3) determining the likelihood of
• intense thirst, and gas accumulation strangulation
• drowsiness generalized malaise Nursing Management
• aching, and a parched tongue Reduce the increasing
• Decompression of the bowel
and mucous membranes. absorption of distention
fluids and
through an NG tube
stimulate more • Assessing for fluid and
gastric secretion electrolyte imbalance
• Monitor nutritional status, and
assessing for manifestations
Intestinal lumen increases consistent with resolution ( return
of normal bowel sounds,
Decrease in venous and arteriolar decreased abdominal distention,
capillary pressure subjective improvement in
abdominal pain and tenderness,
Intestinal lumen increases passage of flatus or stool).

Edema, Congestion, Necrosis, and

Perforation
 -Most obstructions in the large bowel occur in the sigmoid colon.
Large Bowel The most common causes are carcinoma, diverticulitis, inflammatory bowel disorders, and fecal impaction
Obstruction
-If blood supply is cut off, intestinal CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
strangulation and necrosis occur
• Symptoms develop slowly, Diagnostics:
-Dehydration occurs more slowly • Abdominal x-ray
constipation, bloody stool → carcinoma, diverticulitis
-Caused by adenocarcinoid tumors • and abdominal CT or MRI findings
• Iron deficiency anemia inflammatory bowel disorders
• Distended abdomen and fecal impaction Medical Management
crampy lower abdominal pain
-IV therapy, NGT aspiration &
• Fecal vomiting develops decompression
• Shock may occur Blockage in the intestines -Colonoscopy: untwist and decompress
the bowel
-Cecostomy: surgical opening made
Impairment of passage of fecal
into the cecum, urgent relief from
material
obstruction
-Surgical resection: remove the
Distention leading to edema, obstruction
necrosis and perforation of -A temporary or permanent colostomy
bowel -Ileoanal anastomosis, if necessary to
remove the entire large bowel
-Rectal tube used to decompress area
lower in the bowel
Nursing Management
Activation of local and -intestinal tube insertion (miller abott,
systemic local inflammatory cantor tube) for decompression
responses due to bacterial -fluid and electrolyte replacement
invasion through the -prophylactic antibiotic
intestinal mucosal wall -v/s, I&O
-stool exam
-surgery
 Hemorrhoids -Abnormal dilation and weakness of the veins of the anal canal
- Variously classified as Internal or External, Prolapsed, Thrombosed and Reducible
Internal hemorrhoids CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
- These dilated veins lie above
• Internal hemorrhoids- cannot Diagnostic Test:
the internal anal sphincter
be seen on the peri-anal - Anoscopy
- Usually, the condition
area - Digital rectal examination
is PAINLESS
• External hemorrhoids- can Trearments:
be seen Nonsurgical treatments
External hemorrhoids
• Bright red bleeding with • Infrared photocoagulation
- These dilated veins lie below
each defecation • Laser therapy
the internal anal sphincter
• Rectal/ perianal pain Conservative surgical treatment
- Usually, the condition is PAINFUL
• Rectal itching • rubberband ligation procedure
• Skin tags • cryosurgical hemorrhoidectomy
Hemorrhoidectomy
• For advance thrombosed vein

Nursing Interventions:
-Advise patient to apply cold packs to the
anal/rectal area followed by a SITZ bath
-Apply astringent like witch hazel soaks
-Encourage HIGH-fiber diet and fluids
-Administer stool softener as prescribed

Post-operative care for hemorrhoidectomy

-Position: Prone or Side-lying
-Maintain dressing over the surgical site
-Monitor for bleeding
-Administer analgesics and stool softeners
-Advise the use of SITZ bath 3-4 times
a day
INFLAMMATORY BOWEL DISEASE
a group of chronic disorders: Crohn’s disease ( regional enteritis) and ulcerative col
 Crohn’s Disease -- Also called Regional Enteritis
- An inflammatory disease of the GIT affecting usually the distal ileum and colon
- characterized by periods of remission and exacerbation
- Usually first diagnosed in CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
adolescents and young adults
-most commonly occurs in the distal • Fever Diagnostics:
ileum and the ascending colon • Abdominal Crypt inflammation and - Proctosigmoidoscopy initially
distention abscesses - stool exam- maybe (+) for occult blood and steatorrhea
- More often seen among smokers
- barium study of the upper GI tract- is confirmatory w/c
- Etiology: unknown • Diarrhea
- The terminal ileum thickens with shows the classic string sign on x-ray film indicating
• Crampy RLQ
edema formation, with scarring, Formation small, focal ulcers constriction the segment involved
abdominal - CBC, ESR (↑), Albumin and protein (↓)
ulcerations, abscess formation and pain Nursing Management
narrowing of the lumen
• Anorexia/N/V Deepen into longitudinal • Acute phase: Maintain NPO status and administer fluids
Approximately 35% of patients have
• Weight loss and transverse ulcers and electrolytes intravenously or via parenteral nutrition
• Anemia as prescribed.
only ileal involvement (ileitis), 45%
• Restrict the client’s activity to reduce intestinal activity.
of patients have diseased ileum and
• Monitor bowel sounds and for abdominal tenderness and
colon (ileocolitis), and 20% of patients Fistulas, fissures, and
cramping.
have only colon involvement abscesses formation
• Monitor stools, noting color, consistency, and the
(granulomatous colitis)
presence or absence of blood.
• Monitor for bowel perforation, peritonitis and hemorrhage.
- The clusters of ulcers- CLASSIC
• Bowel wall thickens and • Following the acute phase, the diet progresses from clear
COBBLESTONE APPEARANCE
becomes fibrotic liquids to a low-fiber diet as tolerated.
• Intestinal lumen narrows • Instruct the client about diet; usually a lowfiber, high-
protein diet with vitamins and iron supplements are
prescribed.
• Instruct the client to avoid gas-forming foods, milk
Crohn’s Disease products, and foods such as whole wheat grains, nuts,
raw fruits and vegetables, pepper, alcohol, and caffeine-
containing products.
• Instruct the client to avoid smoking.
• Administer medications as prescribed, which may include
a combination of medications such as salicylate
compounds, corticosteroids, immunosuppressants, and
antidiarrheals.
 Ulcerative - Recurrent ulcerative and inflammatory condition of the mucosal and submucosal layers of the colon and rectum
- The colon becomes edematous and develops bleeding ulcerations

Colitis - Scarring develops overtime with impaired water absorption and loss of elasticity
- characterized by unpredictable periods of remission and exacerbation with bouts of abdominal cramps and bloody
or purulent diarrhea.
-inflammatory changes typically CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY MANAGEMENT
begin in the rectum and progress
SEVERE diarrhea (10-20 liquid Genetic factors Diagnostics:
proximally through the colon
stools/day) with Rectal bleeding Immune system reactions - Abdominal X ray
• Weight loss Environmental factors - stool exam- (+) for blood
• Fever NSAID use - ↓ hematocrit and hemoglobin
• Anorexia and Vomiting Low levels of antioxidants and albumin
• Anemia and Hypocalcemia Psychological stress factors - ↑ WBC
Smoking history
• Dehydration - Sigmoidoscopy, colonoscopy
Consumption of milk product
• LLQ Abdominal pain and - Barium enema
cramping - MRI and CT scan Complications
• Tenesmus Impaired microbiota - toxic megacolon,
perforation, bleeding,
Dysregulated mucosal immune
osteoporotic fracture
response
Complications:
• Toxic megacolon
• Multiple ulcerations • Perforation
• Diffuse inflammations • Bleeding
• Desquamation or shedding of the • Osteoporotic fracture
colonic epithelium

Ulcerative colitis
Nursing Interventions (for Chrohn’s Disease and ulcerative Colitis)
1. Maintain NPO during the active phase
2. Monitor for complications like severe bleeding, dehydration, electrolyte
imbalance
3. Monitor bowel sounds, stool and blood studies
4. Restrict activities = rest and comfort
5. Administer IVF, electrolytes and TPN if prescribed (Monitor complications of
diarrhea)
6. Instruct the patient to AVOID gas-forming foods, MILK products and foods
such as whole grains, nuts, RAW fruits and vegetables especially SPINACH,
pepper, alcohol and caffeine
7. Diet progression- clear liquid- LOW residue, high protein diet
8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming
agents and vitamin/iron supplements
 CROHN DISEASE ULCERATIVE COLITIS '.

Bowel region Ileum * colon Colon only

Distribution Skip lesions Diffuse
Stricture Yes Rare
Wall appearance Thick Normal

Inflammation Transmural Limited to mucosa

Pseudopolyps Moderate Marked
Ulcers Deep, lcnife-like Superficial, broad-based
Lymphoid reaction Marked Moderate

lt Fibrosis Marked Mild to none

beginning in rectum Serosiris Marked Mild to none
Granulomas Yes (-35%) No
Fistulae/sinuses Yes No

Perianal fistula Yes (in colonic No

Pseudopolyp Ulcer disease)
Faflvitamin Yes No
malabsorption
malignant With colonic Yes
pntentia involvement
Recurrence after Common No
Transmural inflammation surgery
Ulcerations
 Toxic megacolon No Yes
Fissures
All features may not be present in a single case.
end.