Disorders of The Digestive System Handouts

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DISORDERS OF THE DIGESTIVE SYSTEM

• Disorders of the digestive system have serious consequences for the activity of the organism as a
whole

• Digestive system communicates with the external environment through the intake of fluids and
food

THE MOST COMMON DISORDERS of the digestive system

• Motor dysfunction of smooth muscle of the individual parts of the digestive system -
Aperistalsis refers to a lack of propulsion

• Indigestion of food and absorption of nutrients - malabsorption syndrome

• Bleeding into the individual parts of the digestive tract – hemorrhoids, peptic ulcers, tears or
inflammation in the esophagus, diverticulosis and diverticulitis, ulcerative colitis and Crohn's
disease, colonic polyps, or cancer in the colon, stomach or esophagus.

• Perforation of the wall of the digestive system with subsequent leakage of the contents to the
peritoneal cavity - appendicitis and diverticulitis

• Obstruction in moving of the contents of one part of the digestive system to the next section -
hernias; colon cancer; diverticulitis, Crohn's disease

• Circulation disorders in the wall of the individual parts of the digestive system

CLINICAL MANIFESTATIONS of GI dysfunction

1. Vomiting

• is the forceful emptying of stomach and intestinal contents through the mouth

• the vomiting center lies in the medulla oblongata and includes the reticular formation and
tractus solitarius nucleus

• stimulation of the vomiting center occurs directly by irritants or indirectly.

Cause of:

• the sudden expansion of the stomach and duodenum in the sudden accumulation of contents

• Indirect - reflex response to intense pain - trauma of ovary, testis, uterus, bladder and
kidneys or stimulating the vomiting center, for example. metabolic acidosis or brain lesions

• Direct - irritation of the stomach mucosa by toxic substances

2. Dyspepsia (malfunction of digestion)

• frequently it is functional (non-ulcer) dyspepsia

• dyspepsia similar to ulcer symptomatology: pain predominates

• dyspepsia similar to dysmotility symptomatology: nausea, vomiting, bloating


• For individual diseases of the upper GI, these symptoms can be combined in various ways

Symptoms

abdominal pain

feeling of imperfect digestion

bloating

nausea

Malfunction

esophagus

stomach

duodenum

Disease

peptic ulcer

long-lasting reflux of stomach contents into the esophagus

gastritis

3. Diarrhea

an increase in the frequency of defecation and the fluid content, volume, and weight of feces.

Clinical manifestation

- can be acute or chronic

- systemic effects of prolonged diarrhea – dehydration, electrolyte imbalance (hyponatremia,


hypokalemia), metabolic acidosis, and weight loss

- manifestations of acute bacterial or viral infection - fever, with or without cramping pain, bloody
stools

- Steatorrhea (fat in the stools) and diarrhea are common signs of malabsorption syndrome

Factors determining the stool volume and consistency

• water volume

• the presence of undigested and resorbable food components

• increased production of intestinal secretions

Pathomechanisms involved in the origination of diarrhea

• osmotic activity of intestinal contents


• increased fluid secretion into the lumen of the intestine

• accelerated intestinal peristalsis

Management

• The patient should avoid caffeine,

• carbonated beverages, and

• very hot and very cold foods, because they stimulate intestinal motility

• restrict milk products, fat, whole-grain products, fresh fruits, and vegetables for several days.

• Certain medications (eg, antibiotics, anti-inflammatory agents) and antidiarrheals (eg,


loperamide [Imodium],

• diphenoxylate [Lomotil])

• Loperamide is the medication of choice because it has fewer side effects than
diphenoxylate

• Small-volume diarrhea

− caused by an inflammatory disorder of the intestine, such as ulcerative colitis, Crohn disease, or
microscopic colitis

− inflammation of the colon causes smooth muscle contraction, cramping pain, urgency, and
frequency

• Motility diarrhea

− caused by resection of the small intestine (short bowel syndrome), surgical bypass of an area of
the intestine – diarrhea predominant, diabetic neuropathy, hyperthyroidism, and laxative abuse

− excessive motility decreases transit time, mucosal surface contact, and opportunities for fluid
absorption, resulting in diarrhea

• Osmotic diarrhea (large-volume diarrhea)

− non-absorbable substance in the intestine draws water into the lumen by osmosis => excess of
water and the non-absorbable substance => large-volume diarrhea

− large oral doses of poorly absorbed ions, such as magnesium, sulfate, and phosphate, can
increase intraluminal osmotic pressure

− osmotic diarrhea disappears when ingestion of the osmotic substance stops

− malabsorption related to lactase deficiency, pancreatic enzyme or bile salt deficiency, small
intestine bacterial overgrowth, and celiac disease also cause diarrhea

lactase deficiency
lactose, milk sugar, is not digested by the intestine => high osmotic activity => binds water => increase
in the intestine volume content

• Secretory diarrhea (large-volume diarrhea)

− caused by excessive mucosal secretion of chloride- or bicarbonate-rich fluid or inhibition of net


sodium absorption

− infectious causes include viruses (e.g., rotavirus), bacterial enterotoxins (e.g., E. coli, Vibrio
cholerae ), or exotoxins from overgrowth of Clostridium difficile following antibiotic therapy

4. Constipation

- difficult or infrequent defecation

- it is associated with difficulty emptying of solid stool, which is usually painful

Clinical manifestation (min. two of the following for at least 3 months)

1) straining with defecation at least 25% of the time

2) lumpy or hard stools at least 25% of the time

1) blood in the stools

3) sensation of incomplete emptying at least 25% of the time

1) feeling of bowel fullness and discomfort

4) manual maneuvers to facilitate stool evacuation for at least 25% of defecations

5) fewer than three bowel movements per week

It is resulting from failure of:

✔ transporting the contents (mucus secretion -> colon - motion content)

✔ damage of nerve cells in the intestinal wall - regulation of peristalsis (congenital absence of the
cells - a significant dilatation of the colon)

✔ neurogenic disorders (stroke, PD, spinal cord injury, MS) - neurotransmitters are altered or
neural pathways are degenerated, resulting in delayed colon transit time

✔ endocrine and metabolic disorders associated with constipation (Diabetes mellitus,


hypokalemia, hypercalcemia)

✔ weakened muscles of the abdominal wall - pain after operation

✔ inflamed hemorrhoids in the anal part - during defecation are quite painful

✔ physical activity stimulates peristalsis => sedentary lifestyle and lack of regular exercise are
common causes of constipation

Medical Management
• Bowel habit training,

• increased fiber and

• Daily dietary intake of 25 to 30 g/day of fiber (soluble and bulk-forming) is


recommended,

• fluid intake, and

• Judicious use of laxatives.

• If laxative use is necessary, one of the following may be prescribed: bulk-forming agents,
saline and osmotic agents, lubricants, stimulants, or fecal softeners.

• Enemas and rectal suppositories are generally not recommended for treating

• constipation;

• Routine exercise to strengthen abdominal muscles is encouraged.

• Specific medications may be prescribed to enhance colonic transit by increasing propulsive


motor activity. These may include cholinergic agents.

5. GASTROINTESTINAL BLEEDING

often the result of a large number of diseases

Bleeding in the upper GIT

(esophagus, stomach, duodenum)

esophageal varices

hemorrhagic gastritis

gastric and duodenal ulcers

Bleeding in the lower GIT

(jejunum, ileum, colon, rectum)

inflammation

tumors

Hemorrhoids

sudden and intense bleeding in the GIT is life threatening and manifests the presence of blood in the
stool or vomit

Signs of bleeding in GIT

Hematemesis
presence of blood in vomit, in the form of fresh blood or blood precipitates

blood in vomit in the form of "coffee grounds"

blood flows more slowly in the stomach - it's time for him to digest it - hemoglobin converts to acidic
hematin (black)

Melena

dark stool caused by digested blood

Occult bleeding

chronically recurrent losses of small amounts of blood that usually results in anemia due to iron losses

6. MALABSORPTION SYNDROMES

• malabsorption syndromes interfere with nutrient absorption

• historically malabsorption disorders have been classified as maldigestion or malabsorption

maldigestion

-failure of the chemical processes of digestion (intestinal lumen)

-caused by deficiencies of enzymes (pancreatic lipase, intestinal lactase)

inadequate secretion of bile salts and inadequate reabsorption of bile in the ileum

malabsorption

-failure of the intestinal mucosa to absorb (transport) the digested nutrients

-result of mucosal disruption (gastric or intestinal resection, vascular disorders, or intestinal disease)

- Small intestine excretes certain digestive enzymes and is also the most important area for the
absorption of nutrients

- Resorption area depends on the construction of normal mucosa, which is shaped into the villi.

- Incomplete digestion of food can occur at several levels GIT due to malfunction of secretion of
digestive juices

- celiac and lactose intolerance are considered to be primary diseases of malabsorption in our
geographical area.

✔ Celiac – malabsortion of proteins

- caused by the the allergic response in the small intestine to gluten - a protein present in different
cereals

- resulting inflammation of the mucosa results in villus atrophy => significantly reduced resorption
area/capacity of the small intestine

✔ Lactase Deficiency – malabsorption of sugar


- Lactase - lack of activity - enzyme which degrades lactose (milk sugar) => after the ingestion of milk,
lactose present in the small intestine as an osmotically active agent (binds H2O => greatly increases the
volume of the intestinal contents. In addition, lactose is decomposed by intestinal bacteria to gas and
substances that irritate the mucous membranes.

This results in abdominal cramps, bloating and diarrhea often.

Diagnostic

• Stool studies for quantitative and qualitative fat analysis,

• Lactose tolerance tests,

• D-xylose absorption tests (how well the intestines absorb a simple sugar)

• Schilling tests. (absorbing vitamin B12 properly)

• hydrogen breath test that is used to evaluate carbohydrate absorption

• Endoscopy with biopsy of the mucosa is the best diagnostic tool.

• Biopsy of the small intestine

• Ultrasound studies,

• CT scans, and

• x-ray findings

• complete blood cell count is used to detect anemia.

• Pancreatic function tests

DISORDERS OF THE GIT

A. DYSPHAGIA

• Dysphagia is characterized as swallowing disorders, which may be due to mechanical


obstruction of the esophagus, or functional disorder that impairs esophageal motility

• Mechanical obstruction

- intrinsic - tumor, strictures

- extrinsic - originate outside the esophageal lumen and narrow the esophagus by pressing inward on
the esophageal wall. The most common cause of extrinsic mechanical obstruction is tumor

• Functional dysphagia

- caused by neural or muscular disorders that interfere with swallowing or peristalsis.

- typical causes of functional dysphagia in the upper esophagus - dermatomyositis (a muscle disease)
and neurologic impairments caused by stroke, MS, PD, ALS
ASSESSMENT AND DIAGNOSTIC FINDINGS

• X-ray with a contrast material (barium X-ray)

• Dynamic swallowing study

• Endoscopy (Fiber-optic)

• Esophageal muscle test (manometry)

• Imaging scans

MANAGEMENT

• Esophageal dilation

• Surgery

• Medications (antacids, antibiotics)

B. ACHALASIA

Achalasia is a primary esophageal motility disorder characterized by an inability of the lower


esophageal sphincter to relax and is constantly contracted

Food accumulates in the upper part of the esophagus, which gradually dilates,

ASSESSMENT AND DIAGNOSTIC FINDINGS

• X-rays of your upper digestive system (esophagram)

• Upper endoscopy

• Esophageal manometry

MANAGEMENT

• eat slowly, drink fluids with meals

• oral calcium channel blockers and nitrates

• Calcium channel blockers and nitrates are taken by mouth 10 to 30 minutes before a
meal. For people with achalasia, these medications relax the muscles of the lower
esophageal sphincter, allowing food and liquid to pass more easily into the stomach.

• botulinum toxin (Botox) via endoscopy

• botulinum toxin (Botox) administration of botulinum toxin acts at the neuromuscular


junction to cause muscle paralysis
• pneumatic dilation

• Pneumatic dilation is an endoscopic therapy for achalasia. An air-filled cylinder-shaped


balloon disrupts the muscle fibers of the lower esophageal sphincter, which is too tight
in patients with achalasia.

• Surgical myotomy - This procedure destroys the muscles at the gastroesophageal junction,
allowing the valve between the esophagus and stomach to remain open.

o Heller myotomy

o Peroral endoscopic myotomy (POEM)

C. HIATAL HERNIA

the opening in the diaphragm through which the esophagus passes becomes enlarged, part of
the upper stomach moves up into the lower portion of the thorax

There are two main types of hiatal hernias: sliding and paraesophageal.

1. Sliding, or type I, hiatal hernia occurs when the upper stomach and the gastroesophageal
junction are displaced upward and slide in and out of the thorax.

The patient with a sliding hernia may have pyrosis, regurgitation, and dysphagia.

2. A paraesophageal hernia occurs when all or part of the stomach pushes through the
diaphragm beside the esophagus.

- Paraesophageal hernias are further classified as types II, III, or IV, depending on the extent of
herniation.

- Large hiatal hernias may lead to intolerance to food, nausea, and vomiting.

- Hemorrhage, obstruction, and strangulation can occur with any type of hernia.

ASSESSMENT AND DIAGNOSTIC FINDINGS

• X-ray studies

• Barium swallow

• Esophagogastroduodenoscopy (EGD)

MANAGEMENT

• Frequent, small feedings

• Do not recline for 1 hour after eating

• Elevate the head of the bed on 4- to 8-inch (10- to 20-cm) blocks


• Surgical hernia repair

• Nissen fundoplication (laparoscopic)

D. DIVERTICULUM

An esophageal diverticulum is an out-pouching of mucosa and submucosa that protrudes through a


weak portion of the musculature of the esophagus.

Diverticula may occur in one of the three areas of the esophagus—

• pharyngoesophageal (upper),

• midesophageal (middle), or

• epiphrenic (lower)

CLINICAL MANIFESTATIONS

• Dysphagia

• Fullness in the neck

• Belching

• Belching: Getting rid of excess air. Belching is commonly known as burping.

• Regurgitation of undigested food

• Gurgling noises after eating

• Coughing (when the patient assumes a recumbent position, undigested food is regurgitated)

• The recumbent position describes the body's position when it is lying horizontally, such
as when sleeping.

• Halitosis

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Barium swallow

• Manometric studies

The manometry test senses the pressure and constriction of muscles in the esophagus as you swallow.

• Esophagoscopy is contraindicated

• Blind insertion of an NG tube should be avoided


MANAGEMENT

• Diverticulectomy

• Myotomy of the cricopharyngeal muscle

• Postoperative: evidence of leakage from the esophagus, developing fistula.

• Food and fluids are withheld until x-ray studies show no leakage at the surgical site

E. ESOPHAGEAL PERFORATION

a surgical emergency

may result from iatrogenic causes (endoscopy or intraoperative injury, forceful vomiting or severe
straining, foreign-body ingestion, trauma, and malignancy)

Perforation can occur at the cervical, thoracic, or abdominal portion of the esophagus

CLINICAL MANIFESTATIONS

• excruciating retrosternal pain

• Retrosternal means behind the breastbone, or sternum.

• The esophagus is located in the center of your chest in an area called the mediastinum.

• dysphagia

• Infection,

• fever,

• leukocytosis,

• Leukocytosis means you have a high white blood cell count.

• severe hypotension

ASSESSMENT AND DIAGNOSTIC FINDINGS

• X-ray studies

• Fluoroscopy by either a barium swallow or esophagram (a noninvasive test)

• Chest CT scan

MANAGEMENT

• Requires immediate treatment

• NPO

• Beginning IV fluid therapy


• Administering broad-spectrum antibiotics

• Antifungal therapy

• Surgical repair of the perforation

• Postoperative nutritional status is a major concern (NPO 7 days, parenteral nutrition)

F. GERD

is the reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis.

HCl, pepsin and bile - induce mucosal inflammation, erosion and ulceration

It is a consequence of:

weakened function of the lower esophageal sphincter,

delayed gastric emptying with an increase in the pressure of its content and

weakened clearing function of the esophagus (lack of saliva, poor esophageal peristalsis, and
decreased production of the esophageal mucosal glands).

CLINICAL MANIFESTATIONS

• heartburn,

• chronic cough,

• asthma attacks

• abdominal pain (within 1 hour after meals, repeating)

Heartburn is a burning feeling in the chest caused by stomach acid travelling up towards the
throat (acid reflux).

− symptoms may worsen if the individual lies down, or in the case of increasing intra-abdominal
pressure (as a result of coughing, vomiting, or of hard stool)

− heartburn can be seen as chest pain, which requires the exclusion of cardiac ischemia

− alcohol or foods that contain acid (citrus fruits) can cause discomfort and worsen the
symptoms

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Patient’s history

• Endoscopy or barium swallow


• Ambulatory 12- to 36-hour esophageal pH monitoring

• Ambulatory 12- to 36-hour esophageal pH monitoring is used to evaluate the degree of


acid reflux

G. GASTRITIS

G. Gastritis (inflammation of the gastric or stomach mucosa) is a common GI problem. Gastritis


may be acute, lasting several hours to a few days, or chronic, resulting from repeated exposure
to irritating agents or recurring episodes of acute gastritis

Acute gastritis

• dietary indiscretion—a person eats food that is irritating, too highly seasoned, or
contaminated with disease-causing microorganisms.
• Pharmacologic - overuse of aspirin and other nonsteroidal anti-inflammatory drugs
(NSAIDs), excessive alcohol intake,
• bile reflux,
• radiation therapy.
• Scarring can occur, resulting
• in pyloric stenosis or obstruction.
• major traumatic injuries;
• burns;
• severe infection;
• hepatic, renal, or respiratory failure;
• major surgery

Chronic gastritis

• benign or malignant ulcers


• bacteria Helicobacter pylori
• Autoimmune diseases such as pernicious anemia;
• dietary factors such as caffeine;
• the use of medications such as NSAIDs or bisphosphonates (eg, alendronate [Fosamax],
risedronate [Actonel], ibandronate [Boniva]);
• alcohol;
• smoking; or
• chronic reflux of pancreatic secretions and bile into the stomach
CLINICAL MANIFESTATIONS (ACUTE)

• abdominal discomfort,

• headache,

• lassitude,

• Lassitude is defined as a feeling of lethargy or a lack of mental or physical energy.

• nausea,

• anorexia,

• vomiting, and

• hiccupping

• Hiccups are involuntary contractions of the diaphragm. (which can last from a few
hours to a few days)

CLINICAL MANIFESTATIONS (CHRONIC)

• anorexia,

• heartburn after eating,

• belching,

• a sour taste in the mouth, or

• nausea and vomiting.

• mild epigastric discomfort or

• report intolerance to spicy or fatty foods or slight pain that is relieved by eating.

Patients with chronic gastritis from vitamin deficiency usually have evidence of malabsorption of
vitamin B12 caused by the production of antibodies that interfere with the binding of vitamin B12 to
intrinsic factor.

ASSESSMENT AND DIAGNOSTIC FINDINGS

• upper GI x-ray series

• endoscopy

• histologic examination of a tissue specimen

MANAGEMENT

1. Acute gastritis

- refrain from alcohol and food until symptoms subside.

- a nonirritating diet is recommended.


- If the symptoms persist, intravenous (IV) fluids may need to be administered.

- is caused by ingestion of strong acids or alkalis, To neutralize acids, commo antacids (eg,
aluminum hydroxide) are used; to neutralize an alkali, diluted lemon juice or diluted vinegar is
used.

- If corrosion is extensive or severe, emetics and lavage are avoided because of the danger of
perforation and damage to the esophagus.

2. Chronic gastritis

- modifying the patient's diet,

- promoting rest,

- reducing stress,

- recommending avoidance of alcohol and NSAIDs, and

- initiating pharmacotherapy.

NURSING MANAGEMENT

• Reducing Anxiety

• Promoting Optimal Nutrition

• Promoting Fluid Balance

• Relieving Pain

H. PEPTIC ULCER

H. PEPTIC ULCER

is a result of imbalance between the mucosal defense mechanisms in the esophagus, stomach and
duodenum, and gastric mucosa-damaging mechanisms

relates to digestion of mucous membrane and lower parts of the stomach, duodenum, and lower
esophagus by HCl and pepsin

Risk factors for peptic ulcer disease:

genetic predisposition

H.pylori infection of the gastric mucosa

age greater than 65 years


psychologic stress (mechanism unknown)

excessive use of alcohol

smoking

acute pancreatitis

chronic obstructive pulmonary disease

obesity

Cirrhosis

Types of Peptic Ulcers:

acute - quickly heal by the mucosa regeneration

chronic - penetrate deeper into the tissue, healing takes several weeks or months

Special types of ulcers:

Cushing - traumatic origin, or after surgery CNS (irritation of n. Vagus -> hypersecretion HCl)
Curling - traumatic origin, after burns (↑ levels of histamine -> hypersecretion HCl)
Zollinger - Ellison Syndrome - ↑ production of gastrin -> stimulates the secretion of HCl)
Stress ulcers - mucosal perfusion defect

Clinical Manifestations

Symptoms of an ulcer may last for a few days, weeks, or months and may disappear only to reappear,
often without an identifiable cause.

• dull,

• gnawing pain or

• a burning sensation in the midepigastrium or the back.

• Pain is usually relieved by eating, because food neutralizes the acid, or by taking alkali;
however, once the stomach has emptied or the alkali’s effect has decreased, the pain
returns.

• Sharply localized tenderness can be elicited by applying gentle pressure to the


epigastrium at or slightly to the right of the midline.

• Heartburn (pyrosis)

• Vomiting (emesis)

• constipation or
• diarrhea, and

• bleeding.

• melena (tarry stools).

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Physical examination may reveal pain, epigastric tenderness, or abdominal distention.

• Upper endoscopy

• Serologic testing for antibodies against the H. pylori antigen,

• stool antigen test, and

• urea breath test

• CBCs, FOBT

Management

• Combination of antibiotics, proton pump inhibitors, and sometimes bismuth salts (10 to 14 days)
(e.g., metronidazole [Flagyl] or amoxicillin [Amoxil] and clarithromycin [Biaxin]).

• H2 blockers and proton pump inhibitors (ulcers not associated with H. pylori infection)

• Avoid the use of aspirin and other NSAIDs.

• Smoking cessation

• Dietary modification (to avoid over-secretion of acid and hypermotility in the GI tract)

• Three regular meals a day

• Avoiding extremes of temperature in food and beverages and overstimulation from the
consumption of alcohol, coffee and other caffeinated beverages.

• Surgery

• Vagotomy (VAGUS NERVE - main nerves of your parasympathetic nervous system. This
system controls specific body functions such as your digestion)

• Pyloroplasty - lower part of the stomach (pylorus)

• An antrectomy is the resection, or surgery, of the main stomach referred to as antrum.

I. MORBID OBESITY

Morbid Obesity

- more than two times their ideal body weight or

- BMI exceeds 40kg/m2


- more than 100 pounds greater than ideal body weight

MANAGEMENT

• weight loss diet

• Pharmacologic

• surgical

o A, Roux-en-Y gastric bypass. A horizontal row of staples across the fundus of the
stomach creates a pouch with a capacity of 20 to 30 mL. The jejunum is divided
distal to the ligament of Treitz and the distal end is anastomosed to the new
pouch. The proximal segment is anastomosed to the jejunum.

o B, Gastric banding. A prosthetic device is used to restrict oral intake by creating


a small pouch of 10 to 15 mL that empties through the narrow outlet into the
remainder of the stomach.

o C, Vertical-banded gastroplasty. A vertical row of staples along the lesser


curvature of the stomach creates a new, smaller stomach pouch of 10 to 15 mL.

o D, Biliopancreatic diversion with duodenal switch. Half of the stomach is


removed, leaving a small area that holds about 60 mL. The entire jejunum is
excluded from the rest of the gastrointestinal tract. The duodenum is
disconnected and sealed off. The ileum is divided above the ileocecal junction
and the distal end of the jejunum is anastomosed to the first portion of the
duodenum. The distal end of the biliopancreatic limb is anastomosed to the
ileum.

J. APPENDICITIS

• is an inflammation of the vermiform appendix, which is a projection from the apex of


the cecum

CLINICAL MANIFESTATIONS

Clinical manifestation:

• pain is initially diffuse and poorly localizable (visceral pain), later when the inflammation transit
to the parietal peritoneum, patients localize the pain in the right hypogastrium (somatization
visceral pain)

• the pain may be vague at first, increasing in intensity over 3 to 4 hours

• right lower quadrant pain is associated with extension of the inflammation to the
surrounding tissues

• Psoas sign - elicited by having the patient lie on his or her left side while the right thigh
is flexed backward

• Rovsing sign – referred pain


• nausea, vomiting, and anorexia follow the onset of pain, and

• fever is common

• diarrhea occurs in some individuals, particularly children; others have a sensation

of constipation

• perforation, peritonitis, and abscess formation are the most serious complications of appendicitis

The exact cause of appendicitis is controversial.

• Fecalit - obstruction of the lumen with stool, tumors, or foreign bodies with consequent
increased intraluminal pressure, ischemia, bacterial infection, and inflammation is a common
theory

• regardless of the cause - intraluminal pressure increases (secretion of mucus and fluids
continues), propagation of bacteria and leukocytes continues

• the increased pressure decreases mucosal blood flow, and the appendix becomes hypoxic

• the mucosa ulcerates, promoting bacterial or other microbial invasion with further inflammation
and edema.

• inflammation may involve the distal or entire appendix

Diagnostic

• complete blood cell count - elevated whiteblood cell count with an elevation of the neutrophils.
Abdominal x-ray

• ultrasound studies

• CT scans may

• A pregnancy test may be performed for women

Management

• Antibiotics and IV fluids are administered until surgery is performed.

• Appendicitis with perforation (Laparotomy)

K. INFLAMMATORY BOWEL DISEASE

Ulcerative colitis and Crohn disease are chronic, relapsing inflammatory bowel diseases (IBDs) of
unknown origin

both diseases are associated with genetic factors, alterations in epithelial cell barrier functions,
immunopathology related to abnormal T-cell reactions to microflora and other luminal antigens,
and varying phenotypes

Crohn’s disease - any part of the digestive tract - the most common - terminal part of the ileum
- inflammatory process affects all layers of the wall of the digestive tract ->
ulcerations in the wall, the formation of fistulas and abscesses

Ulcerative colitis - affects colon and rectum

- the process of fibrosis is not intensified

Crohn’s disease

Pathology

Transmural thickening

Deep, penetrating granulomas

Clinical Manifestations

• Bleeding - Usually not, but if it occurs, tends to be mild

• Perianal involvement - Common

• Fistulas - Common

• Rectal involvement - About 20%

• Diarrhea - Less severe

• Abdominal Mass – Common

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Barium series

• Sigmoidoscopy

• Colonoscopy

Management

• Corticosteroids, - anti inflamatory

• sulfonamides - antibacterial

• (sulfasalazine [Azulfidine]) - disease-modifying anti-rheumatic drug (DMARD)

• Parenteral nutrition

Ulcerative colitis

Pathology

• Mucosal ulceration
• Minute, mucosal ulcerations

Clinical Manifestations

• Location - Rectum, descending colon

• Bleeding - Common–severe

• Perianal involvement - Rare–mild

• Fistulas – Rare

• Rectal involvement - Almost 100%

• Diarrhea - severe

• Abdominal Mass – Rare

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Barium series

• Sigmoidoscopy

• Colonoscopy

Management

• Corticosteroids, sulfonamides; sulfasalazine

• Bulk hydrophilic agents

• Antibiotics

Surgical Management

• Continent Ileostomy

• Total Colectomy With Ileostomy (ileal stoma

on the abdominal wall)

• Restorative Proctocolectomy With Ileal Pouch Anal Anastomosis

Nursing Diagnoses

• Diarrhea related to the inflammatory process

• Acute pain related to increased peristalsis and GI inflammation

• Deficient fluid volume related to anorexia, nausea, and diarrhea


• Imbalanced nutrition, less than body requirements, related to dietary restrictions, nausea, and
malabsorption

• Activity intolerance related to generalized weakness

• Anxiety related to impending surgery

• Ineffective coping related to repeated episodes of diarrhea

• Risk for impaired skin integrity related to malnutrition and diarrhea

• Risk for ineffective therapeutic regimen management related to insufficient knowledge


concerning the process and management of the disease

Nursing Interventions

• Maintaining Normal Elimination Patterns

• Reports a decrease in the frequency of diarrheal stools

a. Complies with dietary restrictions; maintains bed rest

b. Takes medications as prescribed

• Relieving Pain

• Has reduced pain

• Maintaining Fluid Intake

• Maintains fluid volume balance

a. Drinks 1 to 2 L of oral fluids daily

b. Has normal body temperature

c. Displays adequate skin turgor and moist mucous membranes

• Maintaining Optimal Nutrition

• Attains optimal nutrition; tolerates small, frequent feedings without diarrhea

• Promoting Rest

• Avoids fatigue

a. Rests periodically during the day

b. Adheres to activity restrictions

• Reducing Anxiety

• Is less anxious
• Enhancing Coping Measures

• Copes successfully with diagnosis

a. Verbalizes feelings freely

b. Uses appropriate stress reduction behaviors

• Preventing Skin Breakdown

• Maintains skin integrity

a. Cleans perianal skin after defecation

b. Uses lotion or ointment as skin barrier

• Monitoring and Managing Potential Complications

• Recovers without complications

a. Electrolytes within normal ranges

b. Normal sinus or baseline cardiac rhythm

c. Maintains fluid balance

d. Experiences no perforation or rectal bleeding

L. INTESTINAL OBSTRUCTION

ILEUS - is a serious condition that can have many causes

• Paralytic ileus - in paralysis, intestinal immobility, intestine vasculature failure, CNS disorders

• Spastic ileus - there is a long spasm of various segments of the intestine

- metabolic disorders, parathyroid diseases, spinal cord injury

- this happens very rarely

1. mechanical obstruction - obstruction in the lumen of the intestine and leads to compression of the
wall

• intussusception,

• polypoid tumors and neoplasms,

• adhesions,

• hernias,

• vascular obstruction - strangulation of blood vessel due to thrombosis or embolism

2. functional obstruction - due to the "paralysis" of the intestinal muscles


CLINICAL MANIFESTATIONS (Small Bowel Obstruction)

• may be colic pain (obstruction of the lumen)

• vomiting and

• abdominal distension

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Abdominal x-ray and

• CT findings

• Laboratory studies (ie, electrolyte studies and a complete blood cell count)

Management

• Decompression of the bowel through a nasogastric tube

• Surgical intervention if completely obstructed, the possibility of strangulation and tissue


necrosis

CLINICAL MANIFESTATIONS (Large Bowel Obstruction)

• constipation may be the only symptom for months.

• the stool is altered as it passes the obstruction that is gradually increasing in size.

• Blood loss in the stool may result in iron deficiency anemia. (hematochezia)

• The patient may experience weakness (Asthenia)

• weight loss, and

• anorexia

• the abdomen becomes markedly distended,

• crampy lower abdominal pain.

• fecal vomiting develops (copremesis)

• Symptoms of shock may occur.

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Abdominal x-ray and

• abdominal CT or

• MRI
• Barium studies are contraindicated.

Management

• Restoration of intravascular volume,

• correction of electrolyte abnormalities, and

• nasogastric aspiration and

• Decompression

• A colonoscopy may be performed to untwist and decompress the bowel.

• Surgical

• A cecostomy, in which a surgical opening is made into the cecum,

• A temporary or permanent colostomy may be necessary.

• An ileoanal anastomosis may be performed if removal of the entire large bowel is


necessary (proctocolectomy)

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