College of Nursing

Care of Clients with Problems in Nutrition and Gastrointestinal

Metabolism and Endocrine, Perception and Coordination,
Acute and Chronic (Theory)

2nd Semester 2020-2021

Week 1: Care of Clients with Problems with Nutrition and Gastrointestinal System

Functions of the Gastrointestinal (GI) System:

1. Process food substances
2. Absorb the products of digestion into the blood
3. Excrete unabsorbed materials
4. Provide an environment for microorganisms to synthesize nutrients, such as Vitamin K

Anatomy and Physiology of the Gastrointestinal (GI) System:

Mouth  Contains the lips, cheeks, palate, tongue, teeth, salivary glands, muscles
and maxillary bones
 Saliva contains the enzyme amylase (ptyalin), which aids in digestion
Esophagus  Collapsible muscular tube about 10 inches (25 cm) long
 Carries food from the pharynx to the stomach
Stomach  Contains the cardia, fundus and pylorus
 Mucous glands are located in the mucosa and prevent autodigestion by
providing an alkaline protective covering
 The lower esophageal (cardiac) sphincter prevents reflux of gastric contents
into the esophagus
 The pyloric sphincter regulates the rate of stomach emptying into the small
intestine
 Hydrochloric acid (HCl) kills microorganisms, breaks food into small particles
and provides a chemical environment that facilitates gastric enzyme
activation
 Pepsin is the chief coenzyme of gastric juice, which converts proteins
into proteoses and peptones
 Intrinsic factor comes from parietal cells and is necessary for the absorption
of vitamin B12
 Gastrin controls gastric acidity
Small intestine  Divided into three parts: duodenum, jejunum and ileum
 Majority of the digestive process is completed in the duodenum and
absorption of food occur primarily in the small intestine
 Nutrient and water move from the lumen of the small intestine into the
blood capillaries and lacteals in the villi. Absorption is by active transport,
osmosis and diffusion
Large intestine  Divided into the following parts: cecum, colon, rectum and anus
 The colon is divided into: ascending, transverse, descending and sigmoid
sections
 Absorbs water and eliminates wastes.
 Intestinal bacteria play a vital role in the synthesis of some B vitamins
and vitamin K

Risk Factors Associated with the Gastrointestinal System:

 Allergic reactions to food or medications
 Cardia, respiratory and endocrine disorders that may lead to slowed GI movement or constipation.
 Chronic alcohol use
 Chronic high stress levels
 Chronic laxative use

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  Chronic use of aspirin or NSAIDs
 Diabetes mellitus, which may predispose to oral candida infections or other GI disorders
 Family history of GI disorders
 Long-term GI conditions, such as ulcerative colitis that may predispose to colorectal cancer
 Neurological disorders that can impair movement, particularly with chewing and swallowing
 Previous abdominal surgery or trauma, which may lead to adhesions
 Tobacco use

DISTURBANCES IN INGESTION

1. GASTROESOPHAGEAL REFLUX DISEASE (GERD)

 The backflow of gastric and duodenal
contents into the esophagus
 The reflux is caused by an incompetent
lower esophageal sphincter (LES), pyloric
stenosis or motility disorder

 Risk Factors:
1. Nicotine
2. High-fat foods
3. Beta-adrenergic agents
4. Xanthine-derivatives
(Theophylline, Caffeine)
5. Ganglionic stimulants
6. Elevated
estrogen/progesterone levels

 Clinical manifestations:
1. Heartburn, epigastric pain
2. Dyspepsia
3. Nausea, regurgitation
4. Pain and difficulty with swallowing
5. Hypersalivation

 Diagnostics:
1. Upper GI tract study (Barium swallow)
 Examination of the upper GI tract under fluoroscopy after the client drinks barium
sulfate
 Pre-procedure: Withhold food and fluids for 8 hours prior the test
 Post-procedure:
a. A laxative may be prescribed
b. Instruct client to increase oral fluid intake to help pass the barium
c. Monitor stools for the passage of barium (stools will appear chalky-white
for 24-72 hours post-procedure) because barium can cause a bowel
obstruction
 Interventions:
1. Instruct client to eat a low-fat diet, avoid coffee, tobacco, beer, milk, foods containing
peppermint or spearmint and carbonated beverages
2. Avoid eating or drinking 2 hours before bedtime
3. Maintain normal body weight
4. Avoid tight-fitting clothes
5. Elevate head of the bed on 6-to-8-inch blocks and elevate upper body on pillows
6. Drugs:
a.
H2 receptor antagonists
b.
Proton pump inhibitors
c.
Prokinetic agents

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 7. Surgical intervention: Nissen fundoplication
 Wrapping of a portion of the gastric
fundus around the sphincter
area of the esophagus

2. ACHALASIA
 Absent or ineffective peristalsis of the distal esophagus accompanied by failure of the
esophageal sphincter to relax in response to
swallowing
 May progress slowly and occurs most often in
people 40 years of age or older

 Clinical Manifestations:
1. Difficulty swallowing
2. Sensation of food sticking in the lower
portion of the esophagus
3. Chest pain and heartburn
4. Spontaneous or intentional regurgitation by
the patient to relieve the discomfort
produced by prolonged distension of the
esophagus by food that will not pass into the stomach

 Interventions:
1. Instruct client to eat slowly and to drink fluids with meals
2. As a temporary measure, Ca-channel blockers and nitrates may be administered.
3. Surgical intervention: Esophagomyotomy – the esophageal muscle fibers are
separated to relieve the lower esophageal stricture

3. HIATAL HERNIA (DIAPHRAGMATIC HERNIA)

 The opening in the diaphragm through which the esophagus passes becomes enlarged, and
part of the upper stomach tends to move up into the lower portion of the thorax

Sliding or Type I Hiatal Hernia Paraesophageal or Rolling Hernia

 Protrusion of the esophagogastric junction  Protrusion of the fundus of the stomach and
into the thoracic cavity and back into the the greater curvature into the thorax next
abdominal cavity in relation to position to the esophagus. The gastric junction
changes remains below the diaphragm

 The primary cause of sliding hiatal hernia  This type of hernia is due to anatomical
is muscle weakness in the esophageal defect
hiatus. This may be due to aging process,
congenital muscle weakness, obesity,

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 trauma, surgery, or prolonged increase in
intraabdominal pressure like heavy lifting
and obesity

 Clinical Manifestations:
1. Heartburns
2. Dysphagia
3. The patient with a paraesophageal hernia usually feels a sense of fullness or chest pain
after eating
4. Abdominal pain
5. Nausea and vomiting
6. Gastric distention, belching, flatulence due to accumulation of gas in the
abdomen caused by impaired motility

 Interventions:
1. Relieve pain by administering antacids
2. Client should assume upright position before and after eating for 1 to 2 hours to prevent
protrusion of the stomach into the thoracic cavity
3. Small frequent feedings to prevent gastric distention
4. Instruct client to eat slowly and chew food properly to reduce gastric motility
5. Avoid foods and beverages that decreases LES pressure like fatty foods,
carbonated beverages, coffee, tea, chocolate and alcohol
6. Drugs:
a. Antacids
b. Antiemetics
c. H2 receptor antagonists
d. Prokinetic agents
e. Proton-pump inhibitors

DISTURBANCES IN DIGESTION

1. PEPTIC ULCER DISEASE (PUD)

 May be referred to as a gastric, duodenal or esophageal ulcer, depending on its location
 PUD is an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the
pylorus (the opening between the stomach and duodenum), in the duodenum, or in the esophagus
 PUD occurs with the greatest frequency in people between 40 and 60 years of age

 Predisposing Factors:
1. Stress
2. Smoking
3. Use of corticosteroids, NSAIDs, alcohol
4. History of gastritis
5. Family history of gastric ulcers
6. Infection with H. pylori

 Complications include hemorrhage, perforation and pyloric obstruction

Duodenal Ulcer Gastric Ulcer

Incidence Age: 30 – 60 Usually 50 and over
Male:Female = 2 – 3:1 Male:Female = 1:1
80% of PUDs are Duodenal 15% pf PUDs are Gastric
Signs, Symptoms and Hypersecretion of stomach acid Normal – hyposecretion of stomach
Clinical Findings (HCl) acid (HCl)
Weight loss may occur
May have weight gain Pain occurs ½ to 1 hour after a meal;
Pain occurs 2-3 hours after a meal; often rarely occurs at night
awakened 1-2 AM Vomiting common

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 Vomiting uncommon

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 May be relieved by vomiting
Ingestion of food relieves pain Ingestion of food does not help,
sometimes increases pain
Hemorrhage less likely than with gastric Hemorrhage more likely to occur than
ulcer, but if present, melena more with duodenal ulcer; hematemesis
common than hematemesis more common than melena
More likely to perforate than gastric
ulcers
Malignancy Possibility Rare Occasionally
Risk factors H. pylori, alcohol, smoking, cirrhosis, stress H. pylori, gastritis, alcohol, smoking use of
NSAIDs, stress

 Diagnostics:
1. Barium swallow
2. Endoscopy
 Also known as Esophagogastroduodenoscopy
 Following sedation, an endoscope is passed down the esophagus to view the
gastric wall, sphincters and duodenum; tissue specimens can be obtained

 Interventions:
1. Relieve pain by administering antacid as prescribed
2. Encourage client to promote a healthy lifestyle
3. The client should avoid the following:
 Fatty foods, coffee, tea, chocolate, cola drinks, spices, alcohol
 Bedtime snacks
 Binge eating
 Large quantities of milk
4. Encourage client to quit smoking
5. Enhance coping through stress therapy
6. Drugs:

Antacids Neutralize HCl Aluminum hydroxide gel

Aluminum carbonate
Aluminum-Magnesium hydroxide
Calcium carbonate
Magnesium hydroxide
Magaldrate
Histamine (H2) Reduce HCl secretion Ranitidine
Receptor Antagonists Cimetidine
Famotidine
Nizatidine
Cytoprotective drug Coats the ulcers and enhances Carafate (Sucralfate)
prostaglandin synthesis
Prostaglandin analogue Replaces gastric prostaglandin. It Cytotec (Misoprostol)
suppresses secretion of gastric acid
Proton-pump Inhibitors Suppress gastric acid secretion Omeprazole
Lansoprazole
Rabeprazole
Pantoprazole
Esomeprazole
Anticholinergics Reduce gastric motility and Atropine sulfate
HCl secretion
H. Pylori Drug treatment Antimicrobials Amoxicillin
Clarithromycin
Metronidazole
Tetracycline

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 7. Surgical Interventions:
Vagotomy Severing of the vagus nerve.
Decreases gastric acid by
diminishing cholinergic stimulation
to the parietal cells, making them
less responsive to gastrin. May be
performed via open surgical
approach, laparoscopy or
thoracoscopy
Pyloroplasty Longitudinal incision is made into
the pylorus and transversely
sutured closed to enlarge the
outlet and relax the muscle
Billroth I Removal of the lower portion of
(Gastroduodenostomy) the antrum of the stomach
(which contains the cells that
secrete gastrin) as well as a small
portion of the duodenum and
pylorus.
The remaining segment is
anastomosed to the duodenum
NCM 116 PRELIMS
May be performed to reduce
gastric acid secretion. A
drainage type of procedure is
usually performed to assist with
gastric emptying (because there
is total denervation of the
stomach). Some patients
experience problems with
feeling of fullness, dumping
syndrome, diarrhea and gastritis
Usually accompanies truncal
and selective vagotomies,
which produce delayed gastric
emptying due to decreased
innervation
May be performed in
conjunction with a truncal
vagotomy. The client may
have problems with feeling of
fullness, dumping syndrome
and diarrhea. Recurrence
rate of ulcer is <1%
pg. 7
 Billroth II Removal of lower portion
(Gastrojejunostomy) (antrum) of stomach with
anastomosis to jejunum. Dotted
lines show portion removed
(antrectomy). A duodenal stump
remains and is oversewn
Dumping syndrome, anemia,
malabsorption, weight loss.
Recurrence rate of ulcer is 10%-
15%

Post-operative Interventions:
1. Monitor vital signs
2. Place in a Fowler’s position for comfort and to promote drainage
3. Administer fluids and electrolyte replacements intravenously as prescribed; monitor
intake and output
4. Assess bowel sounds
5. Monitor NG suction as prescribed
6. Maintain NPO status as prescribed for 1 to 3 days until peristalsis returns
7. Progress the diet from NPO to sips of clear water to 6 small bland meals a day, as
prescribed when bowel sounds return
8. Monitor for postoperative complications of hemorrhage, dumping syndrome,
diarrhea, hypoglycemia and vitamin B12 deficiency

2. GASTRITIS
 Inflammation of the gastric or stomach mucosa
 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 Chronic Gastritis

 Caused by the ingestion of food  Caused by benign or malignant ulcers or by
contaminated with disease-causing the bacteria H. pylori, and also may be caused
microorganisms or food that is irritating or by autoimmune diseases, dietary factors,
too highly seasoned, the overuse of aspirin medications, alcohol, smoking or reflux
or other NSAIDs, excessive alcohol intake,
bile reflux or radiation therapy  Clinical manifestations:
 Clinical manifestations: 1. Anorexia, nausea and vomiting
1. Abdominal discomfort 2. Belching
2. Anorexia, nausea and vomiting 3. Heartburn after eating
3. Headache 4. Sour taste in the mouth
4. Hiccups 5. Vitamin B12 deficiency
5. Reflux

 Diagnostics:
1. Upper GI x-ray series
2. Endoscopy
3. Histologic examination of a tissue specimen
4. Achlorhydria or hypochlorhydria or with hyperchlorhydria

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  Interventions:
1. Acute gastritis is managed by instructing the client to refrain from alcohol and food until
symptoms subside. When the client can take nourishment by mouth, a non-irritating diet
is recommended. If the symptoms persist, IV fluids may need to be administered
2. If gastritis is caused by ingestion of strong acids or alkalis, emergency treatment consists
of diluting and neutralizing the offending agent. To neutralized acids, common antacids
(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
3. Chronic gastritis is managed by modifying the client’s diet, promoting rest, reducing
stress, recommending avoidance of alcohol and NSAIDs and initiating pharmacotherapy.
H. pylori may be treated with selected drug combinations
4. The nurse must always be alert for any indicators of hemorrhagic gastritis and
hypotension. If these occur, the physician is notified, and the client’s vital signs are
monitored as the client’s condition warrants

3. PERITONITIS
 Inflammation of the peritoneum, the serous membrane lining the abdominal cavity and covering
the viscera
 It may be caused by ruptured appendicitis, perforated peptic ulcer, diverticulitis, pelvic
inflammatory disease, urinary tract infection or trauma, bowel obstruction and bacterial invasion.
Peritonitis can also result from external sources such as injury or trauma (gunshot wound, stab
wound) or an inflammation that extends from an organ outside the peritoneal area, such as the
kidney

Common gastrointestinal causes of

peritonitis

 Clinical Manifestations:
1. Diffuse pain which tends to become constant, localized and more intense over the site
of the pathologic process.
2. Abdominal tenderness and distention
3. Abdominal rigidity
4. Nausea and vomiting
5. Diminished peristalsis
6. Paralytic ileus
7. Signs of early shock

 Diagnostics:
1. Elevated WBC
2. Abdominal X-ray and ultrasound
3. CT Scan and MRI
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 4. Peritoneal aspiration and culture and sensitivity studies

 Interventions:
1. Monitor vital signs, intake and output
2. Nasogastric tube insertion
3. The client is placed on the side with knees flexed. This position decreases tension on
the abdominal organs
4. Encourage deep breathing to prevent respiratory complications
5. Peritoneal lavage with warm saline to remove exudates, as ordered
6. Insertion of drainage tubes (Penrose drain, Hemovac, Jackson-Pratt)
7. Fluids, electrolytes and colloid replacement as ordered
8. Antibiotics as ordered
9. Administration of TPN as ordered

DISTURBANCES IN ABSORPTION AND INTESTINAL MOTILITY

1. INFLAMMATORY BOWEL DISEASE (IBD)

 Refers t o two chronic inflammatory GI disorders: Crohn’s disease (Regional enteritis) and
Ulcerative colitis
 The cause of IBD is still unknown. Researchers theorize that it is triggered by environmental
agents such as pesticides, food additives, tobacco and radiation. NSAIDs have been found to
exacerbate IBD. Allergies and immune disorders have also been suggested as causes

Comparison of IBDs
CROHN’S DISEASE ULCERATIVE COLITIS
Course Prolonged, variable Exacerbations, remissions
Pathology
Early Transmural Thickening Mucosal ulceration
Late Deep, penetrating granulomas Minute, mucosal ulcerations
Clinical Manifestations
Location Ileum, ascending colon (usually) Rectum, descending colon
Bleeding Usually not, but if it occurs, tends to be Common-severe
mild
Perianal Common Rare-mild
involvement
Fistulas Common Rare
Rectal involvement About 20% Almost 100%
Diarrhea Less severe Severe
Abdominal mass Common Rare
Diagnostic Study
Findings

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 Barium series Regional, discontinuous skip lesions Diffuse involvement
Narrowing of colon No narrowing of colon
Mucosal edema No mucosal edema
Stenosis, fistula Stenosis rare
Thickening of bowel wall Shortening of colon
Sigmoidoscopy May be unremarkable unless Abnormal inflamed mucosa
accompanied by perianal fistulas
Colonoscopy Distinct ulcerations separated by Friable mucosa with pseudopolyps or
relatively normal mucosa in ulcers in descending colon
ascending
colon
Therapeutic Corticosteroids, sulfonamides Corticosteroids, sulfonamides;
Management (sulfasalazine) sulfasalazine useful in
Antibiotics preventing recurrence
Parenteral nutrition Bulky hydrophilic agents
Partial or complete colectomy, with Antibiotics
ileostomy or anastomosis Proctocolectomy, with ileostomy
Rectum can be preserved in some Rectum can be preserved in only a
patients few patients
Recurrence common
Systemic Complications Small bowel obstruction Toxic megacolon
Right sided hydronephrosis Perforation
Cholelithiasis Cholangiocarcinoma
Hemorrhage
Malignant neoplasms
Pyelonephritis
Nephrolithiasis Nephrolithiasis
Arthritis Arthritis
Retinitis, iritis Retinitis, iritis
Erythema nodosum Erythema nodosum

2. DIVERTICULOSIS AND DIVERTICULITIS

 A diverticulum is a saclike herniation of the lining of the bowel that extends through a defect in
the muscle layer
 Diverticulosis exists when multiple
diverticula are present without
inflammation or symptoms
 A low intake of dietary fiber is considered a
predisposing factor, but the exact cause
has not been identified
 Diverticulitis results when food and bacteria
retained in a diverticulum produce
infection and inflammation that can impede
drainage and lead to perforation or abscess
formation. Diverticulitis may occur as an
acute attack or may persist as a
continuing, smoldering infection

 Clinical Manifestations:
1. Bowel irregularity with intervals of diarrhea, nausea and anorexia and bloating or
abdominal distention
2. When inflamed, cramps, narrow stools and increased constipation or at times intestinal
obstruction
3. Weakness, fatigue and anorexia
4. Acute onset of mild to severe pain the left lower quadrant
5. Fever, chills and leukocytosis
6. If left untreated, can lead to peritonitis and septicemia
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NCM 116 PRELIMS pg. 12
  Diagnostics:
1. Colonoscopy
2. CT scan with contrast agent
3. Abdominal X-rays

 Interventions:
1. Provide bed rest during the acute phase
2. Maintain NPO status or provide clear liquids during the acute phase as prescribed
3. Introduce a fiber-containing diet gradually, when the inflammation has resolved
4. Administer antibiotics, analgesics and anticholinergics to reduce bowel spasms as
prescribed
5. Instruct the client to refrain from lifting, straining, coughing or bending to avoid
increased intra-abdominal pressure
6. Monitor for perforation, hemorrhage, fistulas and abscesses
7. Instruct the client to increase fluid intake to 2500 to 3000 mL daily, unless contraindicated
8. Instruct the client to eat soft high-fiber foods, such as whole grains, the client should
avoid high-fiber foods when inflammation occurs, because these foods will irritate the
mucosa further
9. Instruct the client to avoid gas-forming foods or foods containing indigestible roughage,
seeds, nuts or popcorn, because these food substances become trapped in
diverticula and cause inflammation
10. Instruct the client to consume a small amount of bran daily and to take bulk-forming
laxatives as prescribed to increase stool mass
11. Surgical interventions:
a. Colon resection with primary anastomosis may be an option
b. Temporary or permanent colostomy may be required for increased bowel
inflammation

3. MALABSORPTION SYNDROME
 Malabsorption is the inability of the digestive system to absorb one or more of the major vitamins
(especially A and B12), minerals and nutrients
 Diseases of the small intestine are the most common cause of malabsorption
 Conditions that cause malabsorption can be grouped into the following categories:

Mucosal (transport) disorders causing generalized Celia sprue

malabsorption Regional enteritis
Radiation enteritis
Infectious diseases causing generalized malabsorption Small bowel bacterial
overgrowth Tropical sprue
Whipple’s disease
Luminal disorders causing malabsorption Bile acid deficiency
Zollinger-Ellison Syndrome
Pancreatic insufficiency
Postoperative malabsorption After gastric or intestinal resection
Disorders that cause malabsorption of specific nutrients Disaccharidase deficiency leading
to lactose intolerance

 Clinical Manifestations:
1. Diarrhea
2. Bulky, foul-smelling stools that have increased fat content and are often grayish
3. Abdominal distention and pain
4. Increased flatus
5. Weakness
6. Weight loss
7. Decreased sense of well-being
8. Vitamin and mineral deficiency (easy bruising, anemia, osteoporosis)

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  Interventions:
1. Intervention is aimed at avoiding dietary substances that aggravate malabsorption
and at supplementing nutrients that have been lost
2. Primary disease states may be managed surgically or non-surgically
3. Antidiarrheal agents may be used to decrease intestinal spasms
4. Parenteral fluids may be necessary to treat dehydration

4. INTUSSUSCEPTION
 Telescoping of one portion of bowel into another portion. The
condition results in an obstruction to the passage of intestinal
contents

 Clinical Manifestations:
1. Currant jelly stools
2. Colicky abdominal pain
3. Vomiting of gastric content
4. Bile-stained fecal emesis
5. Hypoactive or hyperactive bowel sounds
6. Tender, distended abdomen with palpable
sausage-shaped mass in the right upper
quadrant

 Interventions:
1. Monitor signs of perforation and shock
2. Hydrostatic reduction (barium enema) as prescribed
a. Antibiotics, IV fluids and decompression via NGT
b. Monitor for the passage of normal, brown stool. This indicates resolution of
intussusception. Notify physician. There will be no more need for surgery
c. Monitor for return of bowel sounds, for the passage of barium, and the
characteristics of stool
3. Administer clear fluids and advance the diet gradually
4. Surgery is required for intussusception if not resolved by barium enema

5. HIRSCHSPRUNG’S DISEASE (Aganglionic Megacolon)

 Absence of ganglionic innervation to the muscle of a section of
the bowel – in most instances, the lower portion of the sigmoid
colon just above the anus
 The absence of the nerve cells means there are no peristaltic
waves in this section to move fecal material through the segment
of intestine
 It is caused by an abnormal gene on chromosome 10

 Clinical Manifestations:
1. Chronic constipation
2. Ribbon-like stools

 Surgical intervention: Repair of aganglionic megacolon involves dissection and removal of the
affected section, with anastomosis of the intestine.

DISTURBANCES IN ELIMINATION
1. HEMORRHOIDS
 Dilated varicose veins of the anal canal
 May be internal, external or prolapsed
 Internal hemorrhoids occur above the
anal sphincter

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  External hemorrhoids occur below the
anal sphincter
 Prolapsed hemorrhoids can become
thrombosed or inflamed
 Hemorrhoids are caused from portal
hypertension, straining, irritation or
increased venous or abdominal pressure

 Clinical Manifestations:
1. Constipation
2. Anal pain
3. Rectal bleeding with defecation
4. Anal itchiness

 Interventions:
1. Apply cold packs to the anal-rectal area followed by sitz baths as prescribed.
2. Apply witch hazel soaks and topical anesthetics as prescribed
3. Encourage a high-fiber diet and fluids to promote movements without straining.
4. Administer stool softeners are prescribed
5. Surgical Interventions:
a. Hemorrhoidectomy – simple resection of the hemorrhoids
b. Sclerotherapy – injection of an irritating chemical into a vein to produce localized
phlebitis and fibrosis, thereby obliterating the lumen of the vein
c. Band ligation – the hemorrhoid is tied off at its base with rubber bands, cutting off
the blood flow to the hemorrhoid. The hemorrhoid will then shrink and fall off within
2-7 days
d. Circular stapling

References:

Pillitteri, A. (2010). Maternal and Child Health Nursing: Care of the Childbearing and Childrearing Family (6th
ed.). Wolters Kluwer Health/Lippincott Williams &amp; Wilkins.

Schwenke, T. (2020). Human digestive system - How it works! (Animation).

https://www.youtube.com/watch?v=X3TAROotFfM.

Silvestri, L. A., & Silvestri, A. E. (2020). Saunders Comprehensive Review for the NCLEX-RN Examination (8th ed.).
Elsevier.

Smeltzer, S. C., Bare, B. G., Hinkle , J. L., & Cheever, K. H. (2010). Brunner & Suddarth's Textbook of Medical-
Surgical Nursing (12th ed.). Wolters Kluwer Health/Lippincott Williams &amp; Wilkins.

Udan, J. Q. (2009). Medical-Surgical Nursing: Concepts and Clinical Application (2nd ed.). Educational
Publishing Hou.

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