Metabolism Disorders

Prepared by Vennesha Anderson RN

Objectives
At the end of this lesson, students should:
know about the terms associated with
gastrointestinal disorders.

understand the difference between types of

gastrointestinal disorders.
Objectives
be knowledgeable about the tests to be used
in diagnosing the different gastrointestinal
disorders.
understand the etiology of the different
types of gastrointestinal disorders.
have a knowledge of the nursing
management
Lower GI Disorders
Lower GI Disorders
Gastroenteritis
Or enteritis, is an inflammation of the
stomach an small intestine
May be caused by bacteria, viruses,
parasites or toxins
Upper GI symptoms such as anorexia,
nausea, and vomiting are common
Gastroenteritis
Diarrhea of varying intensity and
abdominal discomfort are nearly universal
feature of GE
Infectious organism usually enters the body
in contaminated water or food
As a result it is often called “food
poisoning”
Cause acute viral illness
Gastroenteritis
Pathophysiology
Bacterial or viral infection of the GI tract
produces inflammation, tissue damage, and
manifestations by two primary mechanisms
1. the production of exotoxins
Gastroenteritis
Pathophysiology
A number of bacteria produce and excrete
an exotoxin that enters the surrounding
environment (intestinal lumen), causing
damage and inflammation
Gastroenteritis

Pathophysiology
Exotoxins in the GI tract are often referred
to as enterotoxins
They impair intestinal absorption and can
cause secretion of significant amounts of
electrolytes and water into the bowel,
resulting in diarrhea and fluid loss
Gastroenteritis
Pathophysiology
Common bacterial enterotoxins include
those produced by staphylococcus,
Clostridium perfringens, clostridium
botulinum, some strains of escheria coli,
and Vibrio cholerae
Gastroenteritis
Pathophysiology
2. invasion and ulceration of the mucosa
Other bacteria, including some shigella,
salmonella, and escherichia coli species,
damage tissue more directly
Gastroenteritis
Pathophysiology
They invade the intestinal mucosa of the small
bowel or colon, producing microscopic
ulceration, bleeding, fluid exudates, and water
and electrolyte secretion
In some cases, the mechanism of injury is
unclear
It may be a combination of direct and toxic
damage
Gastroenteritis
Manifestations
Gastrointestinal effects
Anorexia, nausea and vomiting
Abdominal pain and cramping
Borborygmi, excessively loud and
hyperactive bowel sounds
Diarrhea
Gastroenteritis
Manifestations
General effects
Malaise, weakness and muscle aches
Headache
Dry skin and mucous membranes
Poor skin turgor
Orthostatic hypotension, tachycardia
fever
Salmonella
Food poisoning caused by ingesting raw or
improperly cooked meat, poultry, eggs, and
diary products contaminated with
Salmonella bacteria
These bacteria cause superficial infection of
the GI tract, rarely invading further
They do not produce a toxin
Salmonella
Symptoms develop 8 – 48 hours after ingesting
the bacteria
Diarrhea may be violent with abdominal
cramping, nausea, and vomiting
A low grade fever, chills, and weakness may
accompany GI manifestations
The disease is usually self-limited, resolving
within 3 – 5 days, although bacterema may
develop
Escherichia coli
Malabsorption syndromes
Malabsorption is a condition in which the
intestinal mucosa ineffectively absorbs
nutrients – including carbohydrates,
proteins, fats, water, electrolytes, minerals,
and vitamins resulting in their excretion in
stool
Multiple different bowel disorders can lead
to malabsorption
Malabsorption syndromes
Disease of the small intestine often cause
malabsorption
Other medical and/or surgical conditions
can result in malabsorption if they affect
digestion or the intestinal mucosa
Primary diseases of the small bowel
mucosa, such as Crohn’s disease, and acute
infections, can lead to malabsorption
Malabsorption syndromes
It may also result from maldigestion,
inadequate preparation of chyme for
absorption
E.g. major gastric resections, pancreatic
disorders with impaired pancreatic enzyme
secretion, and biliary disorders that affect
bile secretion can repair digestion and
absorption of chyme
Malabsorption syndromes
Malabsorption causes common
manifestations resulting from impaired
absorption of chyme and the nutrients it
contains
Predominant GI manifestations include
anorexia, abdominal bloating, diarrhea with
loose, bulky, foul-smelling stools
Malabsorption syndromes
Weight loss, weakness, general malaise,
muscle cramps, bone pain, abnormal
bleeding, and anemia are common systemic
manifestations of malabsorption
Ulcerative colitis
A chronic inflammatory bowel disorder that
affects the mucosa and submucosa of the
colon and rectum
Chronic intermittent colitis (recurrent
ulcerative colitis) is the most common form
of the disease
Its onset is insiduous, with attacks that last
1 to 3 months occurring at intervals of
months to years
Ulcerative colitis
Typically, only the distal colon is affected, with
few systemic manifestations of the disease
These manifestations result from malnutrition
and fluid loss due to poor absorption
Three common malabsorption are sprue,
lactose intolerance, and short bowel syndrome
Ulcerative colitis
Approximately 15% of people with
ulcerative colitis develop fulminant colitis,
with involvement of the entire colon, severe
bloody diarrhea, acute abdominal pain, and
fever
Client with fulminant disease are at high
risks for complications
Ulcerative colitis
Pathophysiology
The inflammatory process of ulcerative
colitis begins at the rectosigmoid area of the
anal canal and progresses proximally
In most clients, the disease is confined to
the rectum and sigmoid colon
Ulcerative colitis
Ulcerative colitis
Pathophysiology
It may progress to involve the entire colon,
stopping at the ileocecal junction
Further tissue damage is caused by
inflammatory exudates and the release of
inflammatory mediators such as prostaglandins
The mucosa is red and edematous due to
vascular congestion, friable and ulcerated
Ulcerative colitis
Pathophysiology
It bleeds easily, and hemorrhage is common
Edema creates a granular appearance
Chronic inflammation leads to atrophy,
narrowing, and shortening of the colon,
with loss of its normal haustra
Ulcerative colitis
Manifestataions
Diarrhea is the predominant symptom of
ulcerative colitis
Stools contain both blood and mucus
Nocturnal diarrhea may occur
Ulcerative colitis
Manifestataions
Mild ulcerative colitis is characterized by
fewer than five stools per day
Severe ulcerative colitis can lead to more
than 6 – 10 bloody stools per day, extensive
colon involvement, anemia, hypovolemia,
and malnutrition
Ulcerative colitis
Manifestations
Rectal inflammation causes fecal urgency
and tenesmus
Left lower quadrant cramping relieved by
defecation is common
Other systemic manifestations include
fatigue, anorexia, and weakness
Ulcerative colitis
Manifestations
Clients with severe disease also may have
systemic manifestations such as arthritis ,
skin and mucous membrane lesions, or
uveitis
Some clients develop thromboemboli, with
blood vessel obstruction due to clots carried
from the site of their formation
Ulcerative colitis
Complications
Include hemorrhage, toxic mega colon, and
colon perforation
Massive hemorrhage may occur with severe
attacks of the disease
The risk for colorectal cancer in increased
in clients with ulcerative colitis
Ulcerative colitis
Complications
When the entire colon is involved the risk is
20 to 30 times greater than for the general
public (Porth, 2002)
After the diagnosis, yearly colonoscopies with
biopsy to detect masses or cell dysplasia re
recommended for clients who have extensive
ulcerative colitis (Tierney et al., 2001)
Crohn’s disease
AKA regional enteritis
A chronic, relapsing inflammatory disorder
affecting the GI tract
Affect any portion of the GI tract from the
mouth to the anus, but usually affects the
terminal ileum and ascending colon
Crohn’s disease
Only the small bowel is involved in about
30% to 40% of clients
The disease is limited to the only colon in
15% to 20% of those affected
Both the small and large intestine are
involved in the majority (Braunwald et al.,
2001)
Crohn’s disease
Pathophysiology
Begins as a small inflammatory aphthoid
lesion (shallow ulcers with a white base and
elevated margin, similar to a canker sore) of
the mucosa and submucosa of the bowel
Crohn’s disease
Pathophysiology
These initial lesions may regress, or the
inflammatory process can progress to
involve all layers of the intestinal wall
The inflammatory process involves the
entire bowel wall (transmural)
Crohn’s disease
Pathophysiology
As the disease progresses fibrotic changes
in the bowel wall cause it to thicken and lose
flexibility
The inflammation, edema, and fibrosis can
lead to local obstruction, abscess
development, and the formation of fistulas
Crohn’s disease
Pathophysiology
Depending on the severity and extent of the
disease, malabsorption and malnutrition
may develop as the ulcers prevent
absorption of nutrients
The ulcerations can also lead to protein loss
and chronic, slow blood loss with
consequent anemia
Crohn’s disease
Complications
Intestinal obstruction
When the bladder is involved, recurrent
urinary tract infection occur
Perforation of the bowel is uncommon but
can lead to generalized peritonitis
Crohn’s disease
Complications
Massive hemorrhage is also uncommon
Long standing Crohn’s disease increases the
risk of cancer of the small intestine or colon
by 5 to 6 time
The cancer risk, however is significantly
lower than the risk associated with
ulcerative colitis
Diagnostic tests
Sigmoidoscopy or colonoscopy
Radiologic examination
Stool examination
CBC with hemoglobin and hematocrit
Serum albumin
Folic acid and serum levels
Liver function test
Peritonitis
Inflammation of the peritoneum
A serious complication of many acute
abdominal disorders
Caused by enteric bacteria entering the
peritoneal cavity through a perforated ulcer,
ruptured appendix, perforated diverticulum,
necrotic bowel, or during abdominal surgery
PID, gallbladder rupture, or abdominal
trauma also can lead to peritonitis
Peritonitis
Caused by enteric bacteria entering the
peritoneal cavity through a perforated ulcer,
ruptured appendix, perforated diverticulum,
necrotic bowel, or during abdominal surgery
PID, gallbladder rupture, or abdominal
trauma also can lead to peritonitis
Peritonitis
Pathophysiology
Results from contamination of the normally
sterile peritoneal cavity by infection or a
chemical irritant
Chemical peritonitis often precedes
bacterial peritonitis
Peritonitis
Pathophysiology
Perforation of a peptic ulcer or rupture of
the gallbladder releases gastric juices
(hydrochloric acid and pepsin) or bile into
the peritoneal cavity, causing an acute
inflammatory response
Bacterial peritonitis usually is caused by
infection by E. Coli which normally inhabit
the bowel
Peritonitis
Pathophysiology
Inflammatory and immune defense
mechanism are achieved when bacteria
enter the peritoneal space
When this occurs, mast cells release
histamine and other vasoactive substances,,
causing local vasodilation and increased
capillary permeability
Peritonitis
Pathophysiology
Polymorphonuclear leukocytes (PMNs, a
type of WBC) infiltrate the peritoneum to
phagocytize bacteria and foreign matter
Fibrinogen-rich plasma exudate promotes
bacterial destruction and forms fibrin clots
to seal off and segregate the bacteria
Peritonitis
Pathophysiology
This process helps limit and localize the
infection, allowing host defenses to eradicate it
Continued contamination, however, leads to
generalized inflammation of the peritoneal
cavity
The inflammatory process cause fluid to shift
into the peritoneal space (third spacing)
Peritonitis
Pathophysiology
Circulating blood volume is depleted,
leading to hypovolemia
Septicemia, systemic disease caused by
pathogens or their toxins in the blood, may
follow
Peritonitis
Manifestations
Depends on the severity and extent of the infection, as
well as the age and general health of the client
Abdominal manifestations
Diffused or local pain
Tenderness with rebound
Boardlike rigidity
Diminished or absent breath sounds
Distention
Peritonitis
Manifestations
Anorexia, nausea and vomiting
Systemic manifestations
Fever
Malaise
Tachycardia
Tachypnea
Restlessness
Confusion or disorientation
Oliguria
Peritonitis
Manifestations
The client often presents with evidence of an
acute abdomen, an abrupt onset of diffuse,
severe abdominal pain
The pain may localize and intensify near the
area of infection
Movement may intensify the pain
The entire abdomen is tender, with guarding or
rigidity of abdominal muscles
Peritonitis
Manifestations
Rebound tenderness may be present over the area
of inflammation
Peritoneal inflammation inhibits peristalsis,
resulting in a paralytic ileus
Bowel sounds are markedly diminished or absent,
and progressive abdominal distention is noted
Pooling of GI secretions may cause nausea and
vomiting
Peritonitis
Manifestations
The older, chronically debilitated, or
immunosuppressed clients may present
with few of the classic signs
Increased confusion and restlessness,
decreased urinary output, and vague
abdominal complaint may be the only
manifestation present
Peritonitis
Manifestations
These clients are at increased risk for
delayed diagnosis, contributing to a higher
mortality rate
Peritonitis
Complications
May be life threatening
The very defense mechanisms designed to
isolate and localize the infection can protect
it from immune responses and systemic
antibiotics
Fibrous adhesions in the abdominal cavity
are a late complication and may lead to
subsequent obstruction
Peritonitis
Complications
Without prompt and effective treatment,
septicemia and septic shock can develop
Fluid loss into the abdominal cavity may
also lead to hypovolemic shock
These potentially lethal complications
require immediate, aggressive intervention
to prevent multiple organ failure and death
Peritonitis
Complications
The overall mortality rate associated with
peritonitis is about 40%
Clients with other medical conditions,
older clients, and those with greater
bacterial contamination have a higher risk
of dying
Peritonitis
Complications
Young people with perforated ulcers or
appendicitis, those with less extensive
bacterial contamination, and those who
receive early surgical intervention have
mortality of less than 10%
Peritonitis
Diagnostic test
WBC is elevated
Blood cultures
Liver and renal function studies and serum
electrolytes
Abdominal x-rays
Paracentesis
Peritonitis
Medication-
Until the infecting organisms have been
identified, a broad spectrum antibiotic against
organisms commonly implicated in peritonitis
prescribed
Once culture results have been obtained,
antibiotic therapy is modified to the specific
organism(s) responsible
Peritonitis
Medications
In addition to antibiotic therapy, analgesics
are usually ordered to promote comfort
Peritonitis
Surgery
Intestinal decompress
Peritonitis
Assessment
Health history
Physical examination
Peritonitis
Diagnoses
Pain deficient fluid volume
Anxiety
Diverticulosis
Diverticulosis
Indicates the presence of a diverticula
More than two thirds are asymptomatic
When manifestations such as episodic pain
(usually left-sided), constipation, and
diarrhea occur, they often can be
contributed to irritable bowel syndrome
Diverticulosis
As the disease progress, abdominal cramping,
narrow stools, increased constipation, occult
bleeding in the stools, weakness, and fatigue may
develop
Complications include hemorrhage and
diverticulitis
A diverticulum may bleed, whether it is inflamed
or not, possibly due to erosion of an adjacent
blood vessel by a fecalith in the diverticulum
Fecal incontinence
Loss of voluntary control of defecation,
occurs less frequently than urinary
incontinence but is no less distressing to the
client
Multiple factors contribute to fecal
incontinence
Fecal incontinence
Physiologic conditions such as diarrhea,
stool impaction, pelvic floor relaxation or
loss of sphincter tone, tumors
and psychologic causes such as depression
and confusion
Bowel incontinence is usually considered a
manifestation of a disorder rather than a
disorder unto itself
Fecal incontinence
Pathophysiology
Causes of fecal incontinence are those that
interfere with either sensory or motor control
of the rectum and anal sphincters
If the external sphincter is paralyzed as a result
of spinal cord injury or disease, defecation
occurs automatically when the internal
sphincter relaxes with the defecation reflex
Fecal incontinence
Pathophysiology
If sphincter muscles have been damaged or
excessive pelvic floor relaxation has
occurred, it may not be possible to override
the defecation with voluntary control
Fecal incontinence
Pathophysiology
Age-related changes in anal sphincter tone
and response to rectal distention increase
the risk for fecal incontinence in older
adults
Resting and maximal anal sphincter
pressures are decreased, particularly in older
women
Fecal incontinence
Pathophysiology
In addition, less rectal distension is needed
to produce sustained relaxation of the anal
sphincter in older females
Nursing care
Assessment
Health history: extent, onset, and duration of
incontinence; identified contributing factors;
history of spinal cord or anorectal injury or
surgery; chronic disease such as diabetes,
multiple sclerosis, or other neurologic
disorders
Physical examination: mental status; general
health; examination of perineal tissues, digital
rectal examination
Nursing diagnoses and interventions
Bowel incontinence
Nurses are often responsible for instituting
bowel training programs and other
measures to manage
Teach caregivers to place the client on a
toilet or commode and provide for privacy at
a certain time of day
Maintain a caring, non judgmental manner
in providing care
Fecal incontinence
Risk for impaired skin integrity
Clean the skin thoroughly with mild soap
and water after each bowel movement
Apply a skin barrier cream or ointment after
each bowel movement
If incontinence pads or briefs are used,
check frequently for soiling and change
when feces is noted
Colostomies
Surgical resection of the bowel may be
accompanied by a colostomy for diversion of
fecal contents
A colostomy is an ostomy made in the colon
 It may be created if the bowel is obstructed
Colostomies

by the tumor, as a temporary measure to

promote healing of anastomoses, or as a
permanent means of fecal evacuation when
the distal colon and rectum are removed
Colostomies
Colostomies take the name of the portion
of the colon from which they are formed:
ascending colostomy, transverse colostomy,
descending colostomy, and sigmoid
colostomy.
Colostomies
Colostomies take the name of the portion
of the colon from which they are formed:
ascending colostomy, transverse colostomy,
descending colostomy, and sigmoid
colostomy.
Colostomies
Colostomies take the name of the portion
of the colon from which they are formed:
ascending colostomy, transverse colostomy,
descending colostomy, and sigmoid
colostomy.
Colostomies
A sigmoid colostomy is the most common
permanent colostomy performed,
particularly for cancer of the rectum.
It is usually created during an
abdominoperineal resection
Colostomies
This procedure involves the removal of the
sigmoid colon, rectum and anus through
abdominal and perineal incisions.
The anal canal is closed ,and a stoma formed from the
proximal sigmoid colon
Stoma usually is located on the lower left quadrant of
the abdomen
Colostomies
When a double-barrel colostomy is
performed two separate stomas are created
The distal colon is not removed , but
bypassed
The proximal stoma, which is functional,
diverts feces to the abdominal wall.
distal stoma, also called the mucus fistula,
expels mucus from the distal colon
Colostomies
It may be pouched or dressed with a 4×4 gauge
dressing
A double barrel colostomy may be treated for
cases of trauma, tumor, or inflammation, and it
may be temporary or permanent.
In a Hartmann procedure, a common
temporary colostomy procedure, the distal
portion of the colon is left in place and is over
sewn for closure
Colostomies
A temporary colostomy may be done to
allow bowel rest or healing, such as
following tumor resection or inflammation
if the bowel
It may also be created following traumatic
injury to the colon, such as a gunshot wound
Colostomies
Anastomosis of the several portions of the
colon is delayed because bacterial
colonization of the colon would prevent
proper healing of the anastomosis.
About 3 to 6 months following a temporary
colostomy, the colostomy is closed and the
colon is reconnected
Colostomies
Clients with temporary colostomies require
the same care as clients with permanent
colostomies .
Ileostomy
Ileostomy
An ostomy made in the ileum of the small
intestine
The colon, rectum, and anus are usually
completely removed (total proctocolectomy
with permanent ileostomy)
The anal canal is closed, and the end of the
terminal ileum is brought to the body
surface through the right abdominal wall to
form the stoma
Ileostomy
A temporary or loop ileostomy may be
formed to eliminate feces and allow tissue
healing for 2-3 months following an IPAA
(ileal pouchanal anastomosis)

A loop of ileum is brought to the body

surface to form a stoma and allow stool
drainage into an external pouch
Ileostomy
When ileostomy is no longer necessary, a
second surgery is performed to close the
stoma and repair the bowel, restoring fecal
elimination through the anus
Activity
Nursing care of the client with an ileostomy
Preoperative care
Post op care
Client and family teaching