Unit V. Gastrointestinal disorders.pptx

Medical Surgical II
Unit II. Gastrointestinal disorders
Time allowed : 16 hrs
BY: Wondwossen Yimam (Msc.N)
Dessie
March/2014
By: Wondwossen Yimam (Msc.N)
Wollo University

Assessment of digestive and gastrointestinal function
Assessment
• Health history and clinical manifestations
• Physical assessment (P/E)
Diagnostic evaluations
• Stool tests
• Breath tests
• Abdominal ultrasonography
• DNA testing
• Imaging studies (X-ray ,Contrast studies, CT scans,& MRI)
• Endoscopy (fibroscopy/esophagogastroduodenoscopy,
anoscopy, proctoscopy, sigmoidoscopy, colonoscopy, small-
bowel enteroscopy, and endoscopy through ostomy.
• Manometry and Electrophysiologic Studies
• Gastric Analysis, Gastric Acid Stimulation Test, and pH
Monitoring
• Laparoscopy (Peritoneoscopy)
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Health history and clinical manifestations
 Complete history, focusing on symptoms common to GI
dysfunctions. These symptoms include pain, indigestion
(discomfort or distress associated with eating), intestinal gas,
nausea and vomiting, hematemesis, and changes in bowel
habits and stool characteristics.
 Information about previous GI disease
 Past and current medication use and any previous treatment
surgery.
 Dietary history to assess nutritional status.
 Questioning about the use of tobacco and alcohol
 Changes in appetite or eating patterns and any examples of
unexplained weight gain or loss over the past year.
 Questions about psychosocial, spiritual, or cultural factors that
may be affecting the patient.
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Bowel sounds with auscultation
 Hyperactive = 5 - 6 sounds heard in less than 30 seconds
 Normal = Sounds heard about every 5 to 20 seconds
 Hypoactive = 1 or 2 sounds in 2 minutes
 Absent = No sounds in 3 to 5 minutes
Abdominal exam steps
 Inspection _Auscultation_ Palpation _ Percussion
EX.
• Hyperactive- In simple, acute mechanical obstruction
- Increased, as from diarrhea or early intestinal obstruction
• Decreased, then absent, as in adynamic ileus and peritonitis.
• Before deciding that bowel sounds are absent, sit down and
listen where shown for 2 min or even longer.
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Stool tests
• Inspecting the specimen for consistency and color
and testing for occult (not visible) blood.
• Special tests, including tests for fecal urobilinogen, fat,
nitrogen, parasites, pathogens, food residues, and
other substances
• Fecal occult blood testing is one of the most
commonly performed stool tests.
o Melena / Tarry black/  upper GI bleeding
o Bright red blood  lower GI bleeding
o Blood streaking on surface of stool 
Lower rectal or anal bleeding
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1. Radiographic diagnostic tests
A) Upper GI studies / upper GI series/:-X-ray of upper
GIT is taken after barium is ingested.
• This enables the examiner to detect any anatomic &
functional derangement of the upper GI organs or
sphincters.
• It also aids in the diagnosis of ulcers, tumors,
regional enteritis, & malabsorption syndromes.
• Barium is tasteless, odorless and completely
insoluble (hence not absorbable) substance &
ingested for upper GIT study also installed rectally
(barium enema) for lower GIT studies
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Barium Sulphate
- Radio contrast(radio-opaque) agent for X-ray
imaging
- Used to see inside of our body
- It appears white on the X-ray film
Oral barium sulphate (barium meal)
• Empty the stomach/free of fluid/
• Take low solid diet for a minimum of 24 hrs
• Adult dose: 0.57 – 2.14 mg/kg (but it varies)
Ex. Adult : 200 – 300 ml , 30-45 minutes before CT
& take an additional 200-300 ml 5-10 minutes prior
to examination
• Shake a bottle for 10 seconds prior to use
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Barium Sulphate ---
Oral barium sulphate (barium meal)
For total bowel opacification
• Drink 250 - 450 ml 1-2 hrs before
examination,& another 250-450 ml 5-10
minutes prior to CT examination.
Barium sulphate (barium enema) lower GI
- Help to examine the large intestine ( colon, rectum)
with fluoroscopy (used to see internal organs in
motion)
- To detect tumors ,cancer, ulcerative colitis,etc
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Upper GI studies---
Patient preparation
• Keep the patient NPO after midnight before the test.
• A laxative may be prescribed to clean out the intestinal tract.
• Withheld all medications
• Patient should not smoke the morning before the procedure
because smoking can stimulate gastric motility.
Procedure:-
• The patient is required to swallow barium under direct
fluoroscopic examination and then films are obtained.
• As the barium descends in to stomach, the position, patency, &
caliber of the esophagus are visualized.
• Fluoroscopic examination next extends to stomach.
• The motility & thickness of the gastric wall & mucosal pattern,
& patency of pylori.
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Upper GI studies---
Post procedure
– Follow up care is needed after the procedure to ensure
that the ingested barium has been completely eliminated.
– Stool must be monitored until they return to their normal
color /the barium will look like clay/
– A laxative or enema may be needed.
• The characteristics of the stool can vary greatly.
Stool is normally light to dark brown
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Lower GI studies
B) Barium enema is given before X-ray is taken
• To detect the presence of polyps, tumor, & other
lesions of the large intestine & to demonstrate any
abnormal anatomy or malfunction of the bowel.
Nursing care for patient
• Instruct the patient to eat low - residue diet 1 to 2 days before
the test.
• Give laxatives/colon washout so that colon is absolutely empty
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2. Endoscopic examinations
A. Upper gastrointestinal fiberoscopy ( Esophago-
Gastro-Duodenoscopy (EGD))
Purposes
o For direct visualization of disease of the esophagus,
gastric, & duodenal mucosa (upper GI hemorrhage,
gastritis, PUD, motility can be evaluated)
o Esophageal & gastric motility can be evaluated
o For collection of secretions & tissue specimens for
further analysis
o For foreign body removal
o Cautery for bleeding point
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Endoscopic examinations---
Patient preparations
 NPO 6-12 hour before the examination
 Spray throat with a local anesthesia, along with IV
diazepam before the scope is introduced
 Atropine may be administered to reduce secretions.
 Position the patient on left lateral position
Post procedure care
 Instructed not to eat or drink until the gag reflex returns (in
1 to 2 hour) to prevent aspiration of foods or fluids in to the
lungs.
 Assess for signs of perforation, such as pain, bleeding,
unusual difficulty swallowing, & an elevated temperature.
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ENDOSCOPY
Absolute contraindications for endoscopy
• Shock , Acute MI , Peritonitis , Acute perforation,
Fulminant colitis
Relative contraindications for endoscopy
– Poor patient cooperation
– Coma (unless the patient is intubated)
– Cardiac arrhythmias or recent myocardial ischemia
– Pts on anticoagulants or chronic NSAID therapy
– Oral iron-containing drugs should be stopped 4 - 5 days
before colonoscopy, b/se certain green vegetables
interact with iron to form a sticky residue that is difficult
to remove with a bowel preparation and interferes with
visualization.
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ENDOSCOPY
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ENDOSCOPY---
B. Lower GI fiberoscopy
• Colonoscopy is direct visual inspection of the
colon to the cecum by means of a flexible fiber
optic colonoscopy
Diagnostic colonoscopy
• Lower GI bleeding
• Colonic & ileo-cecal tuberculosis
• Inflammatory bowel disease & malignancy
Therapeutic colonoscopy
• Polyp-ectomy, foreign body removal, & control of
bleeding by electro coagulation
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Lower GI fiberoscopy---
Patient Preparation
• Patient should take only fluids / for 1 to 3 days prior to the
examination/ or 200cc of Mannitol followed by plenty of water after
one hour to initiates loose motions & clears the bowel or
• Laxatives may be ordered for 2 nights prior to the examination
• Before the examination, a narcotic analgesic may be administered
• Position the patient on the left side with the legs drawn up toward
the chest.
• Monitor cardiac & respiratory function
Post procedure care
• Observe for signs & symptoms of bowel perforation (e.g. rectal
bleeding, abdominal pain or distention, fever, or focal peritoneal signs)
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ANOSCOPY, PROCTOSCOPY, & SIGMOIDSCOPY
• Anoscope - is a rigid scope used to examine the anal canal
• Proctoscope –a rigid scope to inspect the rectum
• Sigmoidscope: - a rigid or flexible scope to inspect the
sigmoid colon
• Colonoscope:- used to examine the rectum and sigmoid colon
into the descending, transverse, and ascending colon
 For evidence of ulceration, tumors, polyps, or other pathologic
processes
Patient preparation
• A warm tape water enema is given until returns are clear.
• Dietary restrictions are not usually necessary
• Sedation is not usually required
Post procedure care
• Monitor the patient for rectal bleeding & signs of intestinal
perforation /EX.. Fever, rectal drainage, abdominal distention, &
pain/
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Sigmoidoscopy
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Gastric analysis/gastric acid stimulation test
Purpose
• To estimate the secretary activity of the gastric mucosa
• To determine the presence/degree of gastric retention due to
pyloric or duodenal obstruction
• For the diagnosis of pernicious anemia- by finding the acid
• For the diagnosis of gastric carcinoma- by discovery of cancer
cells in gastric juice
• To estimate the HCl level & evaluate elevated serum gastrin
level.
– Hyperchlorhydria with elevated gastrin - Zollinger-Ellison
syndrome, PUD
– Hypochlorhydria with elevated gastrin - Pernicious anemia,
Atrophic gastritis, Gastric Ca & if the pt is on anti secretory drugs
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Gastric analysis/gastric acid stimulation test---
• The patient is kept NPO for 8 to 12 hours
• Any medications that affect gastric secretions are
withheld for 24 to 48 hours before the test.
• Smoking is not allowed on the morning before the
test
• The gastric acid stimulation test usually is performed
in conjunction with gastric analysis. Histamine or
pentagastrin is administered subcutaneously to
stimulate gastric secretions
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Gastric analysis/gastric acid stimulation test---
• It is important to inform the patient that this injection may
produce a flushed feeling. The nurse monitors blood pressure and
pulse frequently to detect hypotension.
• Gastric specimens are collected after the injection every 15
minutes for 1 hour and are labeled to indicate the time of
specimen collection after histamine injection.
• The volume and pH of the specimen are measured
• Information to be gained from gastric analysis includes the ability
of the mucosa to secrete HCl
• Pernicious anemia—Secrete no acid under basal conditions or
after stimulation
• Severe chronic atrophic gastritis or gastric cancer—Secrete little
or no acid
• Peptic ulcer—Secrete some acid
• Duodenal ulcers—usually secrete an excess amount of acid
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Disease of the mouth & related structures
Periodontal diseases
Periodentum is the tissue that surrounds & supports the teeth
Gingivitis: is an inflammation of gum
• It is the earliest form of periodontal disease
• This is the most common infection of oral tissue
Causes: - Poor oral hygiene, food debris and bacterial plaque
accumulate
C/M: - Painful, inflamed, swollen gums, usually the gums bleed in
response to light contact
Nursing management
 Brush teeth using a soft toothbrush at least 2 times daily after
each meal
 Avoid alcohol & tobacco products
 Maintain adequate nutrition & avoid sweets
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Periodontal diseases---
Periodontitis
Is an inflammation of the tissue around teeth (tooth –sing)
Cause
- May result from untreated gingivitis
- Poor or inadequate dental hygiene
C/M
 May have bleeding
• Infection
• Loosening of teeth
• Loss of teeth /late/
Treatment
- Instruction of patient in proper oral hygiene.
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Periapical abscess / dento-alveolar abscess/
Def. Pus collection around the apex of the teeth
Acute periapical abscess
• It is usually secondary to a suppurative pulpitis (a pus
producing inflammation of the dental pulp) that arises from
an infection extending from dental caries.
C/M
- Dull, gnawing, continuous pain
- Cellulites, edema of adjacent structures, swollen check, fever,
malaise
Management
- Incision & drainage
- Antibiotic
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Periapical abscess---
Chronic periapical abscess
• It is slowly progressive infection process
• This can progress to a fully formed ‘’blind dental
abscess’’ without the patient’s knowing it.
Diagnosis
x – ray
Management
- Incision & drainage
- Antibiotic
- Tooth extraction
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Dental caries
A gradual pathologic disintegration & dissolution of the tooth &
dentin, with eventual involvement of the pulp.
Etiology
It is the interaction of three factors. These are the presence of:-
 A susceptible tooth surface
 Proper microflora / Streptococcus mutans, Actinomyces viscosus
& Lactobacillus/
 A suitable substrate for the microflora / carbohydrate/
Predisposing factors
• Root exposure, lack of fluoride, inadequate personal hygiene
 Normal fluoride in water = 0.7 mg/litre of water
Mx
- Removal of decay (Polishing & Scaling)
- Restoration
- Tooth extraction
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Stomatitis
It is the inflammation of the mucosa of the oral cavity
Causes
• Emotional or mental stress, fatigue, hormonal factors,
minor trauma (such as biting), allergies, acidic foods and
juices, and dietary deficiencies
• Associated with HIV infection / virus/, bacteria / such as,
syphilis & streptococcal/ and fungus monoliasis
C/M
 Shallow ulcers with white gray center & red border seen in
the inner side of lip & cheek or on the tongue
• It begins with a burning sensations & slight swelling
• Usually heals without a scar
Management
• Proper oral hygiene -Antibiotic - Clotrimazole cream -
Gentian violet application
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Parotitis
Parotitis is an inflammation of the parotid gland
Sialadenitis: inflammation of the salivary glands
Causes
- Virus in children
- Staphylococcus aureus
- Mumps virus most common
Risk factors
- Elderly, acutely ill & debilitated people with decreased
salivary flow due to general dehydration or medications
C/M
- Fever, swelling, tenderness & tense gland
- Pain is felt in the ear & swelling gland interfere with
swallowing ,overlying skin soon becomes red & shiny
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Parotitis---
Medical Management
- Antibiotic (Cloxacillin 500Mg Po Qid for 7 days)
- Massage
- Analgesics
- Incision & drainage of the glands if antibiotic therapy is
not effective.
Nursing Interventions
- Administer ordered medication
- Reassure the patient
- Tepid sponge bathes ,etc.
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Trauma of the mouth & jaw
Fracture of the jaw
Fracture of the jaw area usually include injury to the
soft tissues
Causes
- Trauma:- car accident
- Fall
- Hit by a fist or a flying object
- Pathological
- Osteomyelitis - Large dental cyst or neoplasm
C/M
Malocclusion, asymmetry, abnormal mobility & crepitus
(grating sound with movement) and pain.
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Trauma of the mouth & jaw---
Immediate assessment; and management
• Determine obstruction to air way.
– Remove any obstruction from pharynx, such as broken
teeth, dentures, blood clots or broken bones
– Prepare for emergency tracheostomy
• Control haemorrhage by direct pressure on vessels
supplying the area.
• Administer analgesics to relieve pain & anxiety but
not to depress respiration
• Reassure the patient ,prepare for X-ray
• Position the patient in prone position
• Prepare the patient for reduction & fixation
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Oesophageal diesases
Achalasia
Definition: Lack of relaxation of cardiac sphincter
- It is absent or ineffective peristalsis at distal
oesophagus accompanied by failure of the
oesophageal sphincter to relax in response to
swallowing.
• Narrowing of the oesophagus just above the
stomach results in a gradually increasing dilation of
oesophagus in the upper chest
• It may progress slowly
• Affect mostly persons over 40 years of age
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Achalasia---
C/M
- Difficulty in swallowing both liquids & solids
- Patient has a sensation of food ‘’ sticking’’ in lower
portion of the oesophagus.
- Regurgitation, acid reflux, ulceration
- Chest pain & heart burn
Diagnostic Evaluation
• X-ray – shows oesophageal dilation above the
narrowing at the gastro-esophageal junction
• Barium swallows - Endoscopy
Mx
• Instruct the pt to eat slowly & drink fluids with
meals.
• Surgically by esophagomyotomy
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Hiatus hernia---
• The oesophagus enters the abdomen through an opening
in the diaphragm, & empties at its lower end in to the
upper part of the stomach.
• In hiatus hernia, the opening in the diaphragm through
which the oesophagus passes becomes enlarged & parts
of the upper stomach tends to move up in to lower
portion of the thorax
• It occurs more often in women than men
– Increased intra-abdominal pressure
– Increased age
– Trauma
– Congenital weakness
– Forced recumbent position
– Incompetent distal esophageal sphincter (sliding)
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Hiatus hernia---
C/M: A/ Sliding hiatal hernia (7 times more)
- Heartburn - Regurgitation - Dysphagia - Reflux
- 50 % of patients are a symptomatic
B/ Paraesophageal (rolling) hernia M:F (1:4)
• Dysphagia and postprandial fullness(compression of the adjacent
esophagus by a distended cardia) or asymptomatic.
• Acid reflux usually does not occur, because the gastroesophageal
sphincter is intact.
DX: - X-ray studies, barium swallow, and fluoroscopy
Medical Mx
-Frequent, small feedings that can pass easily through the oesophagus.
- Not to recline for 1 hour after eating,
- Elevate head of the bed (10- to 20-cm) mgt - Similar to GERD
Surgery (15% of patients)
- Paraesophageal hernias require emergency surgery to correct torsion
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Oesophageal diverticula
Defn: - It is an out pouching of mucosa & sub mucosa that
protrudes through a weak portion of the musculature.
It leads to:
- Regurgitation of food
- Acid reflux
- Ulceration
• Diverticula may occur in one of three areas of the
oesophagus: -
1/ Pharyngoeophageal or upper part of oesophagus
2/ Mid-oesophageal
3/ Epiphrenic or lower part of the oesophagus
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Oesophageal diverticula---
C/M
• Difficulty in swallowing
• Fullness in the neck & then complain of belching
• Regurgitation of undigested food
• Pouch, becomes filled with food & fluid
• Halitosis & sour taste in the mouth
• Chest pain
- Barium swallow (Esophagoscopy is contraindicated
because of danger of perforation)
- Surgical removal of Diverticula
Nursing Intervention
• Post operatively feed the pt through NG tube
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Gastric disorders
Acute gastritis
• It is an inflammation of the stomach mucosa.
• It is most often due to dietary problem
Cause: - Ingestion of strong acids or alkalis which may cause the
mucosa to become gangrenous or to perforate.
C/M
• Gastric mucous membrane becomes oedematous & undergoes
superficial erosion; it secretes a scanty amount of gastric juice,
containing very little acid but much mucus.
• Abdominal discomfort, headache, nausea, anorexia, & often
accompanied by vomiting & hiccough.
• It will heal by itself
• Occasionally, haemorrhage may require surgical intervention
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Chronic gastritis
Prolonged inflammation of the stomach may be caused by either
being or malignant ulcers of the stomach, or by Helicobacter pylori (
H. pylori)
Causes
- H. pylori
- Autoimmune (parietal cell changes, leading to atrophy & cellular
infiltration)
Risk factors
- Hot drinks & spices
- Use of drugs & alcohol, smoking
C/M
- Anorexia, sour taste in the mouth, heart burn , belching, nausea
& vomiting
- Endoscopy - Upper GI x – ray series
- Histologic examination
- Serologic testing for antibodies for the H. pylori antigens
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Management
For acute gastritis
- Instruct the pt to refrain from alcohol & food until
symptoms subside.
- Recommend non irritant diet
- If symptom persists, administer fluids parentrally
- Aluminium hydroxide syrup 2 tsp tid
- Nasogastric intubation
- Sedatives
For chronic gastritis
- Modify the pt’s diet - Promote rest
- Reduce stress - Treat H.pylori
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PEPTIC ULCER DISEASE (PUD)
Defns
• It is a mucosal lesion of the stomach or
duodenum or the oesophagus
• It is an excavation (hollowed – out area) formed
in the mucosal wall of the stomach, the pylorus,
the duodenum, or the oesophagus
• It is frequently referred to as a gastric, duodenal,
or oesophageal ulcer, depending on its location
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Gastric ulcer
• Age :- Usually 50 year & over
• Risk factors :- Gastritis, alcohol, smoking, NSAID
• Male: Female: - 2: 1
• Stomach acid: - Normal to: - Hypo secretion
• Vomiting: - Common
• Weight: - Loss may occur
• Pain:- ½ - 1 hour after meal & relived by vomiting
• Perforation: - Less common
• Malignancy :- Uncommon
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Duodenal Ulcer
 Age:- Common b/n 30 – 60 years
 Risk factors:- Alcohol, smoking, blood group O, stress
 Male: Female 3: 1
 Stomach acid: - Hyper secretion
 Vomiting: - Uncommon
 Weight: Gain
 Pain: Occurs 2- 3 hour after meal & relived by food ingestion
 Perforation: - More common
 Malignancy- Common
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PUD---
 Etiology of PUD is poorly understood, but it is
associated with Gm negative H.Pylori
• PUD occurs only in the areas of GI tract that are
exposed to HCL & Pepsin
Predisposition
• Stress or anger - Familial tendency
• Use of NSAIDS, alcohol ingestion & excessive
smoking
• Bacterial infection (H. Pylori )
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PUD---
Pathophysiology
Peptic ulceration depends on the defensive resistance of the
mucosa relative to the aggressive force of secretary activity.
The defensive resistance of the mucosa depends on the following
factors:-
1/ Mucosal integrity & regeneration
2/ Presence of a protective mucus barrier
3/ Adequate b/d flow to the mucosa
4/ Ability of the duodenal inhibitory mechanism to regulate
secretion
- The aggressive factors relate to the presence of Helicobacter
pylori & volume of HCL,pepsin & biliary acid
- Ulceration occurs when aggressive factors exceeds the
defensive one
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PUD---
C/M
- Pain (burning sensation cramp like, gnawing pain) in
the mid-epigastrium or in the back
- Vomiting & nausea
- Constipation & bleeding
- Abdominal distention
Diagnostic evaluation
• P/E, Endoscopy, X-ray, Stool exam for occult blood,
Gastric secretary studies
• Biopsy & culture for H. pylori
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PUD---
Management ( Non drug management)
- Stress reduction & rest, Smoking cessation
- Dietary modification, surgery (if drug mgt fails)
Drug management of PUD
The Drug management has 4 major reasons:-
To eliminate H. Pylori bacteria from the GIT- Antibiotics
 To reduce secretion
o H2 – receptor antagonists Ex. Cimetidine
o Prostaglandin E-Analog Ex. Misoprostel
o Anticholinergics Ex. Dicyclomine hydrochloride
o Proton pump inhibitors Ex. Omeprazole
To neutralize acid (Ex. Antacids)
To protect the mucosal barrier Ex. Sucralfate 1gm po QID
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RX for PUD associated with H. pylori
A. Antibacterial Drugs
First Line
• Amoxicillin 1 gm P.O. bid for 7-14 days. PLUS
• Clarithromycin 500 mg P.O. bid for 7-14 days. PLUS
• Omeprazole 20 mg P.O. bid for 7-14 days
Alternatives ( take with meals except PPI)
• Clarithromycin 500 mg bid for 7-10 days PLUS
• Metronidazole 500mg, P.O. bid 7-10 days PLUS
• Omeprazole 20mg P.O/ bid for 7-10 days
Or Lansoprazole 30 mg bid
Alternatives
Bismuth 525 mg QID sublingual
Metronidazole 250mg, P.O. bid
TTC 500 mg QID -------------------- All for 7 days
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RX for PUD only
First Line (Ethiopia)
• Al (OH)3 (400mg) + Mgsio3 (400mg) = 2- 4 chewable tabs P.O or
(220 mg +195 mg/5ml)10-30 ml between meals & at bedtime for 4
weeks OR
 Cimetidine 400mg P.O bid, with break fast and at night, or 800mg
at night for 4-6wks. (400 bid for 6wks for GU)
(Cimetidine for children = 20-40 mg/kg/d IV or PO
Cimetidine for neonates = 10-20 mg/kg/in 4 divided doses) OR
 Famotidine 40mg P.O. at night for 4-6wks
Alternative (Ethiopia)
• Ranitidine 150mg P.O. bid or 300mg at bedtime for 4-6wks OR
• Omeprazole 20mg P.O. /day for 4wks (DU) or 8wks (GU) OR
• Lansoprazole 30 mg BID
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Drug Mx of PUD---
B. Hypo-secretory agents
Cause reduction in acid secretion. It includes:-
i) H2 – receptor antagonists
Block histamine – stimulated gastric secretion (inhibit
pepsin secretion)
Drugs are: - Ranitidine 150 mg bid X 4-6 wks
- Cimetidine 400 mg BID & 800 mg NOCTE
- Famotidine 40 mg at night X 4-6 wks
ii) Prostaglandin E-Analog (E1 & E2)
= Suppresses secretion of gastric acid & stimulate the
production of cyto-protective mucus
Drug: Misoprostol (Cytoprotective )
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Prostaglandin E-analog---
Uses of Misoprostol
A. For duodenal ulcer
100-200 µgm QID PO for 8 days OR
400 µ gm BID PO for 4- 8 days
B. For gastric ulcer
100-200 µ gm QID PO for 8 days
C. For induction of labour
Initial dose : 25 µ gm intravaginally, then
Subsequent dose: 25 µ gm every 3-6 hrs
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Misoprostol---
D. For PPH
- 200 µ gm PR
- Prophylaxis : 400 µgm PR within 1 min of delivery
E. For abortion (< 12 wks GA)
Adjuct to Mifepristone 400 µ gm on day 3 ( 2
days after Mifepristone 600 mg po stat)
C/I:- For PUD in pregnancy ---- Birth defect??
NB. The use of Misoprostol is limited only for abortion
and PPH in Ethiopia
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Hypo-secretory agents---
iii) Anticholinergics
 Excessive HCL secretion & gastric motility can be
partially prevented by decreasing vagal stimulation
• Anticholinergics, rest & sedation, accomplish this by
blocking the action of acetylcholine on smooth muscles
• This blockage decrease gastric motility & inhibits gastric
secretion in large doses
Drugs: - Dicyclomine hydrochloride 10–20 mg every 4–6
hours as needed
iv) Proton pump inhibitors
Action: - Suppression of acid secretion by inhibiting H+/ K+
ATpase (The enzyme that makes gastric acid)
Drug: - Omeprazole 20 mg bid
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Drug Mx of PUD---
C. Antacids
Action: Buffers & neutralizes acid in GIT
Drugs: - Aluminum hydroxide ,Aluminum magnesium
combinations (Maalox) & Magnesium trisilcate
Ex. 2HCL + Al(OH)2 ___ AlCl2 + 2H2O
But:-Tetracycline, propranolol, Iron salts & digoxin decrease
the absorption of antacid drugs
D. Mucosal barrier & fortifiers
Action: - Stimulate mucus production, which results in
accelerated gastric ulcer healing & prevents digestion by
pepsin
Ex. Sucralfate (Gm/dose) 2 BID ,OR 1QID X 6-8 wks
(Sucralfate 1gm po QID)
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Surgical Mx of PUD
1) Vagotomy:-is performed to eliminate the acid
secreting stimulus
2) Vagotomy with Pyloroplasty - involves cutting the
right & left vagus nerves & widening the existing
exit of the stomach at the pylorus
Pyloroplasty is a longitudinal incision is made into the
pylorus and transversely sutured closed to enlarge
the outlet and relax the muscle
3) Antrectomy -to reduce acid secreting portion of
stomach
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Vagotomy
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Pyloroplasty
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Billroth I (Gastroduodenostomy)
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Billroth II(Gastrojejunostomy)
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Surgical Mx of PUD---
4. Truncal vagotomy
• Severs the right and left vagus nerves as they enter
the stomach at the distal part of the esophagus
- This type of vagotomy is most commonly used to
decrease acid secretions and reduce gastric and
intestinal motility
• Recurrence rate of ulcer is 10 –15%
Wollo University

Indications for gastric surgery
• Intractable ulcer (those who fail to heal after 12
to 16wks of medical Rx)
• Life - threatening hemorrhage
• Perforation
• Obstruction of gastric out let
• Surgical removal/reduction of gastric cancer
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Nursing interventions
Preoperative nursing care for a pt having gastric surgery
• Explain the disease process to the pt
• Identify the patient’s (1) knowledge of events that will occur, (2)
psychological readiness (anxiety)for surgery, and (3) physiologic status
before surgery
• Monitor V/S & obtain written informed consent
• Give antibiotics (if indicated) , Skin preparation
• Analgesics after confirming the diagnosis
• Prepare for P/E,LAB tests (Hgb, B/group Rh,etc) & radiographic tests
• Resuscitate the pt with IV fluids
• Insert NG tube (suction GIT)& catheterize the pt
• Keep the pt NPO, Remove dentures, Jewlery & eye glasses/contact L
• Preoperative teaching(atropine & anesthesia side effects, early
ambulation, frequent positioning, coughing & D breathing ex ,etc)
• Explain when to start fluids(Gag reflex ,bowel sound, flatus)
• Documentation
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Post operative complications of gastric surgery
1. Marginal ulcers
2. Hemorrhage/ perforation/peritonitis/
3. Alkaline reflux gastritis
4. Acute gastric dilation
5. Dumping syndrome
6. Gastro-jejunocolic fistula
7. Pyloric obstruction
Wollo University

Post operative complications---
1. Marginal Ulcers: -
This ulceration may cause scarring & obstruction
2. Hemorrhage :-
Cause: - Splenic injury
- Slippage of a ligature
3. Alkaline reflux gastritis
Cause: - Duodenal contents after gastric surgery in which
the pylorus has been by passed or removed.
4. Acute gastric dilation:-
In the immediate postoperative period, distention of the
stomach produces epigastric pain, tachycardia, &
hypotension.
C/M: - Feeling of fullness, hiccups, or gagging.
Rx: - NG tube insertion & aspiration.
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5. Dumping syndrome
Definition: -
- Physiologic response to rapid emptying of gastric contents into
the jejunum, manifested by nausea, weakness, sweating,
palpitations, syncope, and possibly diarrhea; occurs in patients
who have had partial gastrectomy and gastrojejunostomy.
- This occurs after Gastro-jejunostomy because ingested food
rapidly enters the jejunum without proper mixing in the
jejunum & without the normal duodenal digestive process.
Early manifestations: - Occur 5 to 30 minutes after eating.
- Vertigo - Pallor - Tachycardia
- Palpitation - Syncope - Diarrhea
- Sweating - Nausea
- B/P & PR either rises or fall
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5. Dumping Syndrome---
• Epigastric fullness, distention, discomfort, abdominal
crampy, barborygmi (rumbling in the bowel)
• Tenesmus but has no pain
* Early manifestations, probably caused by rapid
movement of extra cellular fluids into the bowel to
convert the rapidly entering hypertonic bolus into
isotonic mixture. This rapid fluid shift decreases the
circulating blood volume. A jejunum distended with
food & fluid increases intestinal peristalsis & motility.
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* Late manifestations of dumping syndrome
- Occur 2 to 3 hours after eating
- It is due to:-
1) The rapid entry of high carbohydrate food in to the jejunum
2) A rise in blood glucose level
3) Excessive insulin
Later, there is a rapid elevation of blood glucose, followed by
increased insulin secretion. This results in a reactive
hypoglycemia, which also is unpleasant for the patient.
Vasomotor symptoms that occur 10 to 90 minutes after eating
are pallor, perspiration, palpitations, headache, and feelings of
warmth, dizziness, and even drowsiness.
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Nursing interventions for dumping syndrome---
• Advise semi-Fowler’s position for 1/2-1 hour after
the feeding; this position prolongs intestinal transit
time by decreasing the effect of gravity
• Lie down when vasomotor symptoms occur
• Limit the amount of fluid ingested at one time
• Eliminate liquids with meals 1 hour before, or 2
hour after meals
• Drink fluids only between meals, not with meals
• Consume a high-protein, high-moderate fat, and a
low carbohydrate & dry diet. (small, more
frequent meals/d rather than large meals)
Wollo University

Nursing interventions for dumping syndrome---
• Avoid milk, sweets, or sugars (for example, fruit juice,
sweetened fruit, milk shakes, honey, syrup, jelly)
• Administer feedings at room temperature, because
temperature extremes stimulate peristalsis
• If symptoms are severe and not effectively controlled with
dietary measures:- Pectin subcutaneously slows the
absorption of carbohydrates or
• Octreotide 100 -200µg TID, IV/ subcutaneousl / blocks
gastric and pancreatic hormones, which factor into
dumping syndrome symptoms
• Sedatives & antispasmodic (dicyclomine 10–20 mg every
4–6 hours )
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Dumping syndrome---
Complications and nursing implications
• Malnutrition and fluid electrolyte imbalances can
occur due to altered absorption
• Monitor intake and output, laboratory values, and the
client’s weight
• Postprandial hypoglycemia can occur due to excessive
insulin release
• Monitor for signs of hypoglycemia (shakiness,
tachycardia, anxiousness, diaphoresis, hunger).
Provide the client with a carbohydrate source
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6) Gastro-jejunocolic fistula
C/M: - Fecal vomiting - Diarrhea - Weight loss
- Anorexia
*The manifestations are caused by bacterial
overgrowth in the small intestine
7) Pyloric obstruction
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Complications after surgery
Perforation ( DU>GU)
C/F: - abrupt sever pain, tenderness, Rebound
tenderness, guarding
Gastric out late obstruction ( Pyloric Stenosis )
• S/S: - Delayed gastric emptying, Fullness, Vomiting,
Weight loss, Dehydration
Hemorrhage
- PUD is the most common Cause of UGI bleeding
- Occurs in 20% of PUD
- NSAID drugs intake increase risk of bleeding
Wollo University

Gastric surgery---
Postoperative interventions
• Position side lying/Semi-Fowler’s position/
• Assess ABC
• Prepare O2,suction machine, emergency drugs, etc
• Resuscitate the pt
• Check patency of tubes
• Monitor vital signs (record Q.30 minutes)
• Monitor bowel sounds – diminished or absent
• Monitor patency of nasogastric tube
• Intake and output
• Assess & manage pain
• Position the pt Q. 2hrs
• ROM (passive and active exercise/ early ambulation/)
• Cough & deep breathing exercise
• Encourage plenty of fluids/d
• Encourage small & frequent meals
• Wound care
• Administer prescribed drugs
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Potential complications of postoperative patients
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DVT

Acute abdomen
Definition 1
 Acute abdomen denotes any sudden condition
with chief manifestation of pain of recent onset in
the abdominal area which may require urgent
surgical intervention
Definition 2
 An episode of severe abdominal pain with an
acute onset (< 8 hours) that lasts for several hours
or longer and requires medical attention. This can
be new pain or an increase in chronic pain
Wollo University

Acute abdomen---
Classification: The pathologic cause for acute
abdomen can be grouped into:-
1. Inflammatory conditions
- Acute appendicitis - Acute cholecystitis
- Acute salpingitis - Acute diverticulitis
2. Perforations of hollow viscera
-Typhoid perforation of ileum
- Perforation of PUD ( DU or GU )
- Perforation of GI carcinoma
- Traumatic perforation
- Perforation of amoebic colitis
Wollo University

Acute abdomen---
3. Intestinal obstruction
- Strangulated hernia, adhesion, volvulus ,intussusceptions
,tumors, strictures & foreign bodies
4. Hemorrhage
- Ruptured tubal pregnancy ,Traumatic rupture of viscera
especially spleen, Ruptured aortic aneurysm, Ruptured liver
cell carcinoma, etc
5. Acute pancreatitis
6. Colic - Ureteric colic - Biliary colics
7. Other gynecological conditions
- Twisted ovarian cyst - Ruptured graafian follicle
8. Medical conditions that may cause abdominal pain
- Gastro-enteritis, - Dysentery - Gastritis, UTI
Wollo University

Acute abdomen---
Symptoms
o Colicky and intermittent pain ( visceral)
o Continuous pain ( somatic)
o Vomiting
o Fever
o Tachycardia
o Constipation
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Acute abdomen---
Signs: Acute abdomen may present with one or
combination of the following clinical signs
• Abdominal distention, visible peristalsis
• Direct and rebound tenderness, guarding
• Anemia, hypotension
• Toxic with Hippocratic faces
• Absence of bowel sound ( peritonitis)
• Special tests (for signs) are possible
Ex. Psoas sign in appendicitis
Murphy‘s sign in acute cholecystitis
• Dehydration with sunken eyeballs (fluid loss)
Wollo University

Acute abdomen---
Diagnosis
• Clinical
History and physical examination
• Laboratory
Complete blood count, cross match, urine analysis,
serum amylase and electrolytes
• Radiology
Ultrasound and plain film of abdomen
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Acute abdomen---
Management
A. Preoperative preparation
Similar to gastric surgery ???
B. Surgery
Definitive laparatomy according to the cause
Patient monitoring and post operative follow up
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Acute appendicitis
Def: - It is an inflammation of the appendix
• The appendix is a small, finger-like appendage about 10
cm long that is attached to the cecum just below the
ileocecal valve
• The appendix fills with food and empties regularly into the
cecum. Because it empties inefficiently and its lumen is
small, the appendix is prone to obstruction and is
particularly vulnerable to infection (ie, appendicitis)
• Appendicitis results from obstruction, inflammation, and
infection of the appendix
• Obstruction leads to hypoxia, which can result in gangrene
and/or perforation of the appendix. Perforation can result
in the formation of an abscess and/or peritonitis.
Wollo University

Acute appendicitis---
Etiology - Not known
Risk factors
• About 2 % of the population will have appendicitis at some
time in their lives; and teenagers more than adults
• Age (most common b/n 10 & 30 Years)
• Sex (M>F)
• Economic status ( high & middle social class )
Pathophysiology: - Appendix becomes inflamed & edematous
as a result of becoming either kicked or occluded, possibly
by a fecalith, parasites, bacteria, virus , tumor, lymphoid
hyperplasia, or foreign body This cause ischemia & necrosis
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C/Ms
• Mild or cramping, epigastric or periumbilical pain (initial)
• Constant, intense RLQ pain (later)
• Nausea, vomiting, anorexia, constipation
• Psoas sign: abdominal pain that occurs when flexing the hip
when pressure is applied to the Rt knee
• Obturator sign: abdominal pain that occurs when the hip is
rotated
• Rovsing's sign: abdominal pain in the RLQ that occurs with
palpation of LLQ
• Rebound tenderness (pain after deep pressure is applied
and released) over McBurney’s point (located halfway
between the umbilicus and anterior iliac spine)
Wollo University

C/Ms---
• Right sided tenderness on rectal examination
• Muscle rigidity, tense positioning, guarding may
indicate perforation with peritonitis
• Normal to low-grade temperature (highly suggests
peritonitis)
• RLQ pain that decreases with a decrease in right hip
flexion or increases with coughing and movement
may indicate perforation with peritonitis
• Diffused pain if appendix is ruptured
• Diminished bowel sounds indicating peritonitis
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• Complete Hx & P/E
• X-ray may reveal a right lower quadrant density or
localized air -flow levels
• Elevated WBC 10,000 -20,000/mm3 with left shift is
consistent with appendicitis; greater than
20,000/mm3 may indicate peritonitis
• Neutrophil (N = 43-73) > 75%
• Ultrasound may show an enlarged appendix.
Management
• Secure IV fluid & administer antibiotics
• Analgesics can be given after diagnosis is made
• Appendectomy
Wollo University

Nursing Interventions
• Analgesics after the diagnosis is made
• Preventing fluid volume deficit by giving IV fluids
• Antibiotics
• A naso gastric tube
• Avoid laxatives/enemas or application of heat to the
abdomen, which could cause perforation
• Reassure the pt & prevent infection
• Preoperative & postoperative nursing care is the same
as that of pt undergoing major surgery
- After surgery, the nurse places the patient in a semi-
Fowler’s position
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Preoperative
• Upon admission, maintain NPO status due to the
possibility of emergency surgery
• Administer IV fluids as prescribed
• Encourage semi-Fowler’s position to facilitate abdominal
drainage in the lower abdomen
Postoperative
• Administer opioid analgesia (usually morphine sulfate 5-
30 mg po 4hlry) as ordered
• Administer IV antibiotics as ordered (surgical
prophylaxis, perforation)
• For peritonitis, monitor nasogastric (NG) tube drainage
• For perforation or abscess, monitor surgical drains
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Complications
• Perforation of appendix (incidence 10 - 32 %) peritonitis &
appendial abscess
- Perforation generally occurs 24 -48 hours after the onset of
pain
- Peritonitis due to perforation is a life-threatening
emergency
Nursing Implications
Carefully assess the client for signs of peritonitis
- Fever > 38.2° C
- Acutely ill appearance
- Board-like abdomen (Guarding)
- Decreased urinary output
- Septicemia
RX:- Broad spectrum IV antibiotics
Wollo University

Chronic inflammatory bowel disease
It is used to designate two chronic inflammatory GI disorders:-
1. Ulcerative colitis
= Large intestine ( colon, sigmoid,& rectum)
- Diarrhea, blood, mucus,& pus
- Only mucosa & sub mucosa layers are involved
- There are continuous lesions
2. Regional enteritis (Crohn's disease)
= Small intestine (esophagus- iIeum )common in ileum
= May affect the large intestine
- Diarrhea without blood
- All layers of the bowel are involved
- There are skip lesions
Wollo University

Ulcerative colitis
- It is a recurrent ulcerative & chronic inflammatory disease of the
mucosal layer of the large intestine, commonly in the sigmoid and
rectal (100%) areas.
- The peak incidence is between 30 and 50 years of age. It is a serious
disease, accompanied by systemic complications and a high mortality
rate
- Eventually, 10 - 15% of the patients develop carcinoma of the colon
• Ulcerative colitis affects the superficial mucosa of the colon and is
characterized by multiple ulcerations, diffuse inflammations, and
desquamation or shedding of the colonic epithelium
• Bleeding occurs as a result of the ulcerations
• Ulcerative colitis: edematous, inflamed mucosa with multiple
abscesses beginning in the rectum and moving upward through the
large intestine
• The disease process usually begins in the rectum and spreads
proximally to involve the entire colon
Wollo University

Ulcerative colitis---
Etiology - Unknown /Genetic, immunologic, & stress/
Predisposing factors:- - Anxiety - Tobacco - Radiation
C/M
• If ulcerative colitis persists for more than 10 years, cancer
may develop
• Severe diarrhea , with blood, pus, and mucus
• Intermittent tenesmus, and rectal bleeding
• Fecal urgency, LLQ cramping
• Anorexia, weight loss, fever, vomiting, and dehydration
• Hypocalcemia and anemia frequently develop
• Extraintestinal symptoms include skin lesions (eg, erythema
nodosum), eye lesions (eg, uveitis), joint abnormalities (eg,
arthritis), and liver disease
• Rebound tenderness may occur in the LLQ
• Periods of exacerbation & remissions
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Clinical presentation of ulcerative colitis---
Signs and symptoms---
• Abdominal cramping
• Frequent bowel movements, often with blood in the stool
• Weight loss
• Fever and tachycardia in severe disease
• Blurred vision, eye pain, and photophobia with ocular involvement
• Arthritis
• Raised, red, tender nodules that vary in size from 1 cm to several
centimeters
 Physical examination
• Hemorrhoids, and fissures, or perirectal abscesses may be present
• Iritis, uveitis, episcleritis, and conjunctivitis with ocular involvement
• Dermatologic findings with erythema nodosum, pyoderma gangrenosum,
or aphthous ulceration
 Laboratory tests
• Decreased hematocrit/hemoglobin
• Increased erythrocyte sedimentation rate
• Leukocytosis and hypoalbuminemia with severe disease
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Diagnostic evaluation
- Careful stool exam: - To r/o amoeba
- The stool is positive for blood
- Low Hgb , Elevated WBC & ESR
- Low albumin levels, and an electrolyte imbalance
- Biopsy with colonoscopy, barium enema, and abdominal X-ray
Mx
• Low fiber diet (Low-residue)
• Reduce or eliminate lactose containing foods
• Avoid caffeinated beverages, pepper, alcohol, cold
foods & smoking
• Oral fluids, vitamins B12 & iron supplement
• Provide high-calorie, high-protein, low-fat
Wollo University

MGT---
- Avoid any food which exacerbate diarrhea & treat
dehydration
- Antibiotics
• Surgery is indicated for fistula formation,
intestinal obstruction, bowel perforation,
hemorrhage, and intractable disease
• Partial or complete ileostomy or anastmosis
◗ Intestinal resections may need to be performed
repeatedly
◗ Ileostomy is curative; ileorectal anastomosis may
be performed
Wollo University

MGT----
• An anticholinergic is used to manage intestinal spasms
• Antidiarrheal (Loperamide 4mg po then, 2mg Q loose stool,
Diphenoxylate + atropine 5mg po tid, or Bismuth
subsalicylate 30 ml prn ) to control diarrhea
• Anti-inflammatory such as sulfasalazine 500 mg, 2-6
gm/d to reduce inflammation
• Antimicrobial to prevent infection (Metronidazole or
Ciprofloxacin )
• Corticosteroid to decrease inflammation
• Immunosuppressant to decrease antigen-antibody reactions
(Ex. Cyclosporine 4 mg/kg per day IV continuous infusion )
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Complications
• Perforation, hemorrhage, malignant neoplasm
• Toxic megacolon: usually involves transverse colon which
dilates and lacks peristalsis (manifestations: fever,
tachycardia, hypotension, dehydration, change in stools,
abdominal cramping)
• Increased risk for colorectal cancer (20 – 30 times); need
yearly colonoscopies
• Abscess, fistula formation
• Bowel obstruction
• Extra-intestinal complications
– Arthritis
– Ocular disorders
– Cholelithiasis
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Ostomy
- Surgically created opening between intestine and
abdominal wall that allows passage of fecal material
- Stoma is the surface opening which has an appliance
applied to retain stool and is emptied at intervals
Name of ostomy depends on location of stoma
Ileostomy: opening in ileum; may be permanent with
total proctocolectomy or temporary (loop ileostomy)
Continent (or Kock’s pouch) ileostomy: has intra-
abdominal reservoir with nipple valve formation to allow
catheter insertion to drain out stool
Ileostomies: always have liquid stool which can be
corrosive to skin since contains digestive enzymes
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Surgical management
– 25 % of patients require a colectomy
– Total proctocolectomy with a permanent ileostomy
• Colon, rectum, anus removed
• Closure of anus
• Stoma in right lower quadrant
– In selected patients an ileo-anal anastomosis or ileal reservoir to
preserve the anal sphincter
• J-shaped pouch is created internally from the end of the ileum to
collect fecal material
• Pouch is then connected to the distal rectum
– Total colectomy with a continent ileostomy
• Kock’s ileostomy
• Intra-abdominal pouch where stool is stored until client drains it with
a catheter
– Total colectomy with ileoanal anastamosis
– Removes colon and rectum and sutures ileum into the anal canal
Wollo University

Regional enteritis
• Regional enteritis, also known as Crohn’s disease
(Granulomatous colitis), is an inflammatory disease of the
small bowel that also may affect the large intestine;
• It typically begins in the ileum but can affect all areas of
the small intestine and even the esophagus
• Crohn’s disease: intermittent involvement throughout the
entire GI tract, most commonly in the small intestine and
the terminal ileum.
• Regional enteritis is a sub acute and chronic inflammation
that extends through all layers (ie, transmural lesion) of
the bowel wall from the intestinal mucosa. It is
characterized by periods of remissions and exacerbations.
Wollo University

Regional enteritis---
Signs and symptoms
- Often continuous or episodic diarrhea; liquid or
semi-formed
- Fever, fatigue, malaise, weight loss, anemia
- Patient with regional enteritis typically has
diarrhea without visible blood
• Lesions are not in continuous contact with one
another and are separated by normal tissue
• Onset of symptoms is usually insidious, with
prominent RLQ abdominal pain and diarrhea
unrelieved by defecation.
Wollo University

Clinical presentation of crohn's disease
(Granulomatous colitis )
 Signs and symptoms
• Malaise and fever
• Abdominal pain (RLQ)
• Frequent bowel movement
• Fistula
• Weight loss
• Arthritis
 Physical examination
• Abdominal mass and tenderness
• Perianal fissure or fistula
 Laboratory tests
• Increased WBCs and ESR
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Diagnosis and treatment
o Small bowel X-ray, barium study of the upper GI tract,
barium enema, and intestinal biopsy
o Restrict raw fruits ,vegetables ,fatty and spicy foods
o Anticholinergic, antidiarrheal, anti-inflammatory
,antimicrobial, corticosteroid, immunosuppressant
o Surgery is indicated for fistula formation, intestinal
obstruction, bowel perforation, hemorrhage, and
intractable disease
- Intestinal resections may need to be performed repeatedly
- Ileostomy is curative; ileorectal anastomosis may be
performed
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MGT
• Aminosalicylate Ex. Sulfasalazine 500 mg 2-6 gm/d
= Salicylate compound that inhibits prostaglandin
production to reduce inflammation or
• Corticosteroids
• Immunosuppressive agents (Cyclosporine 4 mg/kg per
day IV continuous infusion ) for clients who do not
respond to steroid therapy alone
– Used in combination with steroid treatment and may
help decrease the amount of steroid use
• Metronidazole or Ciprofloxacin
– For the fistulas that develop
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MGT---
• Anti-diarrheal medications (Loperamide,
Diphenoxylate/Atropine, or Bismuth subsalicylate )
- Loperamide : Adults: 4 mg initially, then 2 mg after each
subsequent loose stool; maximum 16 mg in 24 hours
- Diphenoxylate + Atropine Adults: Two tablets (5 mg)
initially, then one tablet every 3–4 hours, not to exceed
20 mg in 24 hours
• Bismuth subsalicylate Adults: 30 mL (regular strength)
or 2 tablets, repeated every acute diarrhea 30–60
minutes as needed, Maximum 8 doses daily.
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• Make sure the patient understands the purpose, therapeutic
effects, and adverse effects of prescribed medications
• Provide postoperative care for a patient undergoing surgery
• Maintain patency of the NG tube, if present, by irrigating
with normal saline solution every 2 hours as needed
• Encourage the patient to use patient-controlled analgesia, or
administer an opioid analgesic to relieve pain; administer a
steroid to prevent adrenal insufficiency and an antibiotic to
prevent infection
• Monitor vital signs every 1 to 2 hours for 4 to 8 hours and
then every 4 hours
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Dietary management
• Individualized according to client; eliminate irritating
foods
• Dietary fiber contraindicated if client has strictures
• With acute exacerbations, client may be made NPO
and given enteral or total parenteral nutrition (TPN)
Surgery
Performed when necessitated by complications or failure
of other measures removal of diseased portion of the
bowel
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Complications of regional enteritis
• Intestinal obstruction caused by repeated
inflammation and scarring causing fibrosis and
stricture
• Stricture formation
• Perianal disease
• Fluid and electrolyte imbalances
• Malnutrition from malabsorption
• Fistulas lead to abscess formation; recurrent urinary
tract infection if bladder involved
 Perforation of bowel may occur with peritonitis
• Massive hemorrhage
• Increased risk of bowel cancer (5 – 6 times)
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Intestinal obstruction
• Intestinal obstruction exists when blockage prevents the
normal flow of intestinal contents through the intestinal
tract
• It can be classified as the following:-
A) Mechanical obstruction Vs functional obstruction
Mechanical obstruction: Intussusceptions, polypoid tumors,
stenosis, strictures, adhesions, hernias, and abscesses.
Functional obstruction: amyloidosis, muscular dystrophy,
endocrine disorders(Ex. diabetes mellitus), neurologic
disorders such as Parkinson’s disease
B) Small bowel obstruction Vs large bowel obstruction
C) Partial obstruction Vs complete obstruction
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Small bowel obstruction
Pathophysiology
• Intestinal contents, fluid, and gas accumulate above
the intestinal obstruction
• The abdominal distention and retention of fluid
reduce the absorption of fluids and stimulate more
gastric secretion
• With increasing distention, pressure within the
intestinal lumen increases, causing a decrease in
venous and arteriolar capillary pressure
• This causes edema, congestion, necrosis, and eventual
rupture or perforation of the intestinal wall, with
resultant peritonitis.
Wollo University

Small bowel obstruction---
Pathophysiology
• Reflux vomiting may be caused by abdominal
distention.
• Vomiting results in a loss of hydrogen ions and
potassium from the stomach, leading to a
reduction of chlorides and potassium in the
blood and to metabolic alkalosis.
• Dehydration and acidosis develop from loss of
water and sodium. With acute fluid losses,
hypovolemic shock may occur.
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Causes
- Most bowel obstructions occur in the small intestine(75%)
• Adhesion (1st)of intestinal wall due to surgery & intestinal
tuberculosis
• Hernia (2nd)
• Tumor (3rd)
• Inflammatory condition of intestine
• Paralytic ileus
- Absence of bowel sound & flatus, abdominal distention,
accumulation of air and fluid & infection (Mgt: Nasogastric
tube + Antibiotic + Resuscitation)
• Gallstones ileus
• Ascaris bolus
• Intussusception
Wollo University

C/Ms
• Abdominal cramp (colicky)
• Vomiting early S/S
• Constipation late S/S
• Abdominal distention,DHN
• The patient may pass blood and mucus, but no fecal
matter and no flatus
• Vomiting occurs. If the obstruction is complete,
• Peristaltic waves initially become extremely vigorous
and eventually assume a reverse direction, with the
intestinal contents propelled toward the mouth
instead of toward the rectum.
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C/Ms---
• If the obstruction is in the ileum, fecal vomiting takes place.
First, the patient vomits the stomach contents, then the
bile-stained contents of the duodenum and the jejunum,
and finally, with each paroxysm of pain, the darker, fecal-like
contents of the ileum.
• The unmistakable signs of dehydration become evident:
intense thirst, drowsiness, generalized malaise, aching, and
a parched tongue and mucous membranes.
• The lower the obstruction is in the GI tract, the more
marked the abdominal distention. If the obstruction
continues uncorrected, hypovolemic shock occurs from
dehydration and loss of plasma volume.
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Assessment and diagnostic findings
• Hx ,& P/E
• CBC, Hgb
• Abdominal x-ray
- Show abnormal quantities of gas, fluid, or both
in the bowel
• Laboratory studies
- Electrolyte studies and a complete blood cell
count reveal a picture of dehydration, loss of
plasma volume, and possible infection)
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Medical management
• Decompression of the bowel through a nasogastric
tubes
• Triple Antibiotics
• Intravenous therapy (to replace the depleted water,
sodium, chloride, and potassium)
• Surgical intervention Ex.
- Hernia-- repairing
- Adhesion--- dividing the adhesion to which the
intestine is attached
- Removal of some portion of intestine &
anastomosis performed
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Nursing management
• Maintaining the function of the nasogastric tube
• Keep the pt NPO
• Assessing and measuring the nasogastric output
• Monitor intake and output
• Assessing for fluid and electrolyte imbalance
• Monitoring nutritional status, and
• Assessing improvement (eg, return of normal bowel
sounds, decreased abdominal distention, subjective
improvement in abdominal pain and tenderness,
passage of flatus or stool)
• Nursing care of the patient after surgical repair of a
small bowel obstruction is similar to that for other
abdominal surgeries
Wollo University

Large bowel obstruction
Pathophysiology
• Large bowel obstruction results in an accumulation of
intestinal contents, fluid, and gas proximal to the
obstruction
• Obstruction in the large bowel can lead to severe
distention and perforation unless some gas and fluid
can flow back through the ileal valve.
• Large bowel obstruction, even if complete, may be
undramatic if the blood supply to the colon is not
disturbed.
Wollo University

Large bowel obstruction---
Pathophysiology
• If the blood supply is cut off, however, intestinal
strangulation and necrosis this condition is life
threatening.
• In the large intestine, dehydration occurs more
slowly than the small intestine because the colon
can absorb its fluid contents and can distend to a
size considerably beyond its normal full capacity.
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Causes
- About 15% of intestinal obstructions occur in the
large bowel
• Colorectal cancer (Sigmoid colon)
• Diverticulitis
• Inflammatory bowel disorders
• Benign tumor
• Adhesion
• Paralytic Ileus
• Volvulus
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Hernia
Def.:-It is a protrusion of bowel through a weak
point in the musculature of the anterior
abdominal wall or an existing opening.
Def.:- Hernia is a protrusion of a viscus through an
opening in the wall of the cavity
Etiology
- Powerful muscular effort or strain
- Weakness or defect to the wall of abdominal
cavity
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Hernia---
Risk factors
 Increased intra abdominal pressure resulting from:
• Chronic cough
• Straining at urination or defecation
• Heavy wt lifting
• Abdominal distension/constipation
• Ascites
 Weakened abdominal wall
• Advanced age
• Malnutrition
• Congenital defect
• Trauma/ previous abdominal surgery
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Hernia---
Classification based on sites of hernia
• Inguinal hernia
• Femoral hernia
• Para-umbilical hernia
• The sac of the hernia is a continuation of the
peritoneum of the abdomen.
• The hernial contents are intestine, omentum, or
other abdominal contents that pass through the
hernial opening into the hernial sac.
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Para-umbilical hernia
Risk factors: Female sex, multiple parities,
obesity, & ascites
- These occur just above or below the umbilicus.
Treatment
1/ Expectant: - Spontaneous closure is expected in
80% cases of umbilical hernia in under five
children
2/ Surgery: - Beyond five years
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Hernia---
• Epigastric hernia
-These pass through linea alba above the umbilicus
• Incisional hernia
- These follow breakdown of muscle closure after
previous surgery. If obese, repair is not easy
Risk factors: Wound infection, poor surgical technique
(improper facial repair), chronic cough or straining, &
obesity
Treatment:- Hernioplasty
• Umbilical hernia
- Results from failure of umbilical orifice to close
- Occur most often in obese women & children & in
patients with cirrhosis and ascites.
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Hernia---
Inguinal hernia
- The protrusion of bowel through the weak point is the
inguinal canal which contains the spermatic cord in the
male & the round ligament in the female
• Accounts for 80 % of all external abdominal wall hernia
• Commonest is all ages and sexes
• 20 times more common in males than women
• More common on right side
Inguinal canal
• In male: Spermatic vessels, vas deference, Ileo inguinal
nerve, genito femoral nerve
• In female: Round ligament
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Inguinal canal boundaries
• Anteriorly: External oblique apponeurosis
• Posteriorly: Fascia transversalis
• Inferiorly: Inguinal ligament
• Superiorly: Conjoined tendon and internal
oblique muscle
NB. Risk of obstruction and strangulation is very
high in femoral hernia, paraumblical hernia and
indirect inguinal hernia with narrow neck
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Hernia---
Inguinal hernia
A) Direct inguinal hernia
• Push their way directly forward through posterior wall
of the inguinal canal, into a defect in the abdominal
wall
• Due to wear and tear associated with advanced age
and increased intra abdominal pressure
• Less common (20%)
• Strangulate rarely
Distinguishing direct from indirect hernias
• The best way is to reduce the hernia & occlude the
internal ring with 2 fingers.
• Ask the pt. to cough - if the hernia is restrained it is
indirect; if it pops out it is direct.
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Hernia---
Inguinal hernia
B) Indirect inguinal hernia
• Pass through the internal inguinal ring & then
through the external ring
• Can strangulate
• Common (80%)
• 60% on right, 40% Lt side and 20% bilateral
• Due to congenital defect or potential defect
which is the remnant of processes vaginalis
• 20 times more common in men
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Hernia---
Femoral hernia
• Acquired downward protrusion of intestinal
contents into the femoral canal
• Bowel enters the femoral canal, presenting as a
mass in the upper middle thigh or above the
inguinal ligament where it points down the leg,
unlike an inguinal hernia which points to the groin.
• 4 times more common in females (middle-aged
multiparous)
• It is frequently strangulate & irreducible
• Rare in children
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Anatomy of femoral canal
• Is a narrow rigid space bounded by:-
- Inguinal ligament, superiorly
- Pectineal part of inguinal ligament posterior
- Lacunar part of inguinal ligament medially,
femoral vein laterally
- The narrow rigid space makes this types of hernia
more prone to obstruction and strangulation.
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Hernia---
Classification of hernia according to severity
• Reducible hernia
The protruding mass can be replaced in abdomen
• Irreducible hernia (incarcerated & strangulated)
The protruding mass cannot be moved back into abdomen
• Incarcerated
An irreducible hernia in which the intestinal flow is completely
obstructed.
• Strangulated
An irreducible hernia in which the blood & intestinal flow is
completely obstructed
• Richter’s hernia- when only one side of the wall of the
intestine is herniated. Here strangulation of the bowel can
occur with out intestinal obstruction
• Sliding hernia- when an extra peritoneal structure form part of
the wall of the sac
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Hernia---
C/F of strangulation
- Pain, Vomiting - Swelling of hernial sac - Fever
- Lower abdominal pain
- Sign of peritoneal irritation
Treatment
Mechanical ( For reducible hernia only)
- A truss is an appliance having a pad that is held snugly in the hernial orifice
- It does not cure a hernia - it prevents abdominal contents from entering hernial
sac
Surgical
- Recommended to correct the hernia before strangulation occur which then
becomes on emergency situation.
A/ Hernial sac, is dissected free
B/ Contents of sac, are replaced in abdominal cavity
C/ Neck of sac is ligated
D/ Muscle and fascial layers are sawed together firmly
E/ Strangulated hernia requires resection of ischemic bowel in addition to hernia
repair
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Hernia---
Non operative treatment
• Gentle reduction (taxis) can be indicated in obstructed hernia in
infants but not advisable in adults due to the risk of mass
reduction.
Procedure (taxis)
• Put patient in head down position
• Sedative is given
• Gentle manipulation to reduce the hernia
NB: No place for vigorous manipulation and be ready to stop the
procedure when any difficulty arises
Urgent surgery is indicated in
• Great majority of obstructed hernia and
• All strangulated hernia
Surgery
1. Herniotomy - removal of the sac and closure of the neck: Done
only in infants and children
2. Herniorrhaphy - Herniotomy and repair of the wall to prevent
recurrence.
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Large bowel obstruction
Clinical manifestations
• Abdominal cramp
• Constipation is early S/S
• Grossly distended abdomen
• Fecal vomiting
• Large bowel obstruction differs clinically from small bowel
obstruction in that the symptoms develop and progress
relatively slowly
• In patients with obstruction in the sigmoid colon or the
rectum, constipation may be the only symptom for days.
Eventually, the abdomen becomes markedly distended,
loops of large bowel become visibly outlined through the
abdominal wall, and the patient has crampy lower
abdominal pain.
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Assessment and diagnostic findings
• HX
• P/E
• CBC, Hgb ,etc
• Abdominal x-ray studies (flat and upright) show
a distended colon
• Barium studies are contraindicated
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Medical management
• A colonoscopy may be performed to untwist and decompress the
bowel
• A cecostomy, in which a surgical opening is made into the cecum,
may be performed for patients who are poor surgical risks and
urgently need relief from the obstruction. The procedure provides
an outlet for releasing gas and a small amount of drainage
• A rectal tube may be used to decompress an area that is lower in
the bowel. The usual treatment, however, is surgical resection to
remove the obstructing lesion.
• If there is gangrene rectal tube is C/I
• A temporary or permanent colostomy may be necessary
• An ileoanal anastomosis may be performed if it is necessary to
remove the entire large colon.
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Nursing management
• Keep the pt NPO
• Assessing for fluid and electrolyte imbalance
• Monitoring nutritional status
• Monitor symptoms for intestinal obstruction
• Provide emotional support and comfort
• Administers intravenous fluids and electrolytes as
prescribed
• If the patient’s condition does not respond to
nonsurgical treatment prepare the patient for
surgery
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Disorders of the rectum
Hemorrhoids (Piles)
Def: - It is an enlarged & congested patch of mucosa &
sub-mucosa at ano-rectal junction
- Hemorrhoids are dilated sub mucosal veins in the anus
Hemorrhoid based on its site:-
• Internal hemorrhoids (Internal to the anal orifice)
- If it is above internal sphincter
- Internal hemorrhoids are frequently arranged in three
groups at 3, 7 and 11 o’clock positions
• External hemorrhoids (External to the anal orifice)
- If it is outside external sphincter
• Intero-external hemorrhoids (prolapsed internal
hemorrhoids)
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Hemorrhoids
Classifications of hemorrhoid based on its stage
(severity)
• 1st degree:- Bleed but no prolapsed
• 2nd degree :- Prolapsed but reduces spontaneously
• 3rd degree :- " but need manual replacement
• 4th degree: - " not returned
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Hemorrhoids---
Etiology
Idiopathic
- Chronic constipation
- Excessive use of purgative
- Pelvic masses (pregnancy)
- Portal HTN
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Internal hemorrhoids
Etiology
Though most hemorrhoids are idiopathic, they
may also be secondary to underlying causes,
which include:-
• Straining accompanying constipation
• Straining at micturition
• Recto sigmoid mass
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Internal hemorrhoids---
C/Ms
• Rectal bleeding: is the main and earliest symptom
which is usually slight painless bright red occurring
on passing stool as a splash into the toilet or toilet
papers or covering the stool at the end of
defication
• Prolapse of the varicose masses is a late
manifestation
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C/Ms---
• A mucoid discharge frequently accompanies
prolapsed hemorrhoids and is due to mucus
secretion from the engorged mucus membrane
• Pruritus ani-due to the discharge and perianal
soiling accompanying prolapsed hemorrhoids
• Pain- is not a significant feature of uncomplicated
internal hemorrhoids
• Anemia-due to persistent/profuse bleeding
Wollo University

C/Ms---
Hemorrhoids are graded based on the degree of prolapse
and reducibility in to:
⇒ First degree hemorrhoids: those confined to the anal
canal (do not prolapse out side the anal canal)
⇒ Second degree hemorrhoids: prolapse on defecation
but reduce spontaneously or are replaced manually and
stay reduced.
⇒ Third degree hemorrhoids: prolapse, even apart from
defecation, and remain permanently prolapsed outside
the anal margin. These give rise to a feeling of heaviness
in the rectum
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• Proctoscopy- to visualize internal hemorrhoids
and exclude other lesions
Complications
• Profuse hematochezia, strangulation which leads
to an acute pain, thrombosis, which makes the
mass swollen, dark, tense and feel solid and
tender on examination
• Unrelieved strangulation/thrombosis may lead to
ulceration of the exposed mucus membrane
Gangrene- may lead to spreading of infection/
sepsis and abscess formation
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Conservative measures which include:
• High fiber-diet for a regular soft and bulky motion
• Advice high - residue diet that contain fruit
• Hydrophilic creams or suppositories
EX. Calcium polycarbophil: 1000 mg QID or after each loose
stool, not to exceed 12 tablets per day
• Local application of analgesic ointment /suppository
• Regulating bowel by laxatives
• Avoid constipation
• Sitz bath
• Good p/hygiene ,& avoiding excessive straining during
defecation
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Operative treatment
Hemorrhoidectomy indicated for:-
• Third degree hemorrhoids
• Failure of non-operative treatment of second
degree hemorrhoids
• Fibrosed hemorrhoids
• Intero-external hemorrhoids with well defined
external hemorrhoid
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Treatment of complications
Strangulation, thrombosis and gangrene
 Immediate surgery under adequate antibiotic cover
or adequate pain relief, bed rest, frequent hot sitz
bath, warm saline compress with firm pressure
followed by ligation or excision or anal dilation.
 Severe hemorrhage
o Resuscitation with IV fluids
o Local compression with adrenaline solution
o Pain relief when present
o Blood transfusion when needed
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Conservative Surgical Rx of internal Hemorrhoid
Rubber - band ligation procedure
• The hemorrhoid is visualized through the anoscope, &
its proximal portion above the muco-cutaneous lines is
grasped with an instrument
• A small rubber band is then slipped over the
hemorrhoid. Tissue distal to the rubber band
becomes necrotic after several days & sloughs off
• It may cause infection, pain & hemorrhage
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Conservative surgical Rx of internal hemorrhoid
 Cryosurgical hemorrhoidectomy
• Involves freezing the tissue of the hemorrhoid for a
sufficient time to cause necrosis. It is not used
widely because the discharge is very foul-smelling &
wound healing is prolonged
Hemorrhoidectomy, or surgical excision, can be
performed to remove all of the redundant tissue
involved in the process
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External hemorrhoids
• A thrombosed external hemorrhoid (perianal
hematoma), is usually associated with
considerable pain. It appears as an inflamed tense
tender and easily visible on inspection of the anal
verge
Treatment
• Relieving pain by local or oral analgesics and avoid
constipation
• Surgical evacuation of the clot can be done under
local anesthesia
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Ano-rectal abscess
Def: - It is an infection in the para-rectal spaces
Risk factors
- Regional enteritis
- Immuno-defcient states (HIV/AIDS)
* Many of these abscesses will result in fistulas
C/M
• Abscess may occur in a variety of spaces in & around the
rectum
• Pain
• Foul smelling pus
• In superficial abscess, (swelling, redness & tenderness)
• Deeper abscess ( fever, abdominal pain )
• Fistula
Mx :- 1) Palliative Rx:- Sitz Bath -Analgesic
2) Surgical Rx:- Incision/drainage & antibiotics
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Anal fistula
Anal fistula It is a tiny, tubular, fibrous tract that extends into
the anal canal from an opening located beside the anus
Causes
• Fistula usually results from an infection - Trauma -
Fissures - Regional enteritis
C/M
• Pus or stool may leak constantly from the cutaneous
opening
• Passage of flatus or feces from the vaginal or bladder
depending on the fistulas tract
• Fever
Mx
• Surgery is always recommended
• Fistulectomy (excision of the fistulous tract)
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Anal fissure
Anal fissure: It is a longitudinal tear or ulceration in the lining of
the anal canal
Cause
- Trauma of passing a large firm stool
- Persistent tightening of the anal canal secondary to stress or
anxiety (leading to constipation)
- Child birth/Trauma
C/Ms
• Characteristic sharp, severe pain starting during defecation
and lasting an hour or more and ceases suddenly to reappear
during the next bowel motion
• Constipation
• Bleeding: usually appearing as bright streaks on the stool
surface or the toilet paper
• Extremely painful defecation
• Burning & bleeding
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Anal fissure---
Mx
• A high fiber diet and high fluid intake with a mild laxative, such
as liquid paraffin, to encourage passing of soft, bulky stools
• Administration of a local anesthetic ointment or suppository
• Increase water intake - Sitz bath
• Emollient suppositories
• Corticosteroid suppositories relieve discomfort
*Most of the fissures will heal by conservative measures
Surgical Measures
• In chronic fissures with fibrosis, a skin tag or a mucous polyp
or recurrent anal fissures.
• Lateral anal sphincterotomy and
• Fissurectomy
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Colostomy
Colostomy: - Is the surgical creation of an opening
(stoma) into the colon
- It allows for the drainage or evacuation of colon
contents to the outside of the body.
Colostomy irrigation
a) It is done to permit escape of feces when there is
an obstruction of the large bowel or a known
lesion, such as cancer, that will eventually cause an
obstruction
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Colostomy---
Colostomy irrigation
b) It also may be done to permit healing of the bowel
distal to it after an infection, perforation or
traumatic injury since it diverts the fecal stream
from the affected area
c) It may be done as a palliative measure in the
treatment of an obstruction caused by an inoperable
growth of the colon or if the rectum must be
removed to treat cancer
d) It may be done to provide a permanent means of
bowel evacuation
Wollo University

Colostomy---
Purpose of colostomy irrigation
• To encourage a bowel motion in a recently
established colostomy and to ensure that the
opening is patent
• To relieve constipation in patients who has
difficulty managing their colostomy
• To teach the patient how to establish regularity of
evacuation through the colostomy
• To reduce distention before closure of colostomy
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Placement of permanent colostomies
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Functions of the liver
1. Produce many enzymes
- Detoxification of harmful substances
Ex 1. Alcohol – converted to-- Acetate (For cell respiration)
Ex 2. Drugs ----- Less harm
Ex 3. Ammonia ---Urea
2. CHO metabolism
- Regulate blood glucose( glycogenesis & glycogenlysis)
- Glucose ----- from fructose & galactose
3. Protein metabolism (albumin synthesis)
- 12 non essential amino acids
- Deamination
4. Fat metabolism
- Forms lipoproteins, synthesize cholesterol (increase level
excreted to the bile to be eliminated in the feces)
- Ketones produces ATP for cell respiration
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Functions of the liver---
5. Produces clotting factors
- Prothrombin ,fibrinogen, F-VIII
6. Formation of bilirubin
7. Phagocytosis by kupffer cells
- Destroy old Rbcs &
- Destroy colon bacteria by portal circulation
8. Storage
- Vit A, D,E,K,B12,Iron, Copper
• In the colon some bilirubin is changed to
urobilinogen by the colon bacteria
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Pathways of circulation
1. Pulmonary: Right ventricle →pulmonary artery →
pulmonary capillaries (exchange of gases) →
pulmonary veins → left atrium
2. Systemic: Left ventricle → aorta → capillaries in
body tissues → superior and inferior caval veins
→right atrium
3. Hepatic portal circulation: blood from the
digestive organs and spleen flows through the
portal vein to the liver before returning to the
heart
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Portal circulation
• Blood from the abdominal digestive organs and spleen
circulates through the liver before returning to the
heart
• Blood from the capillaries of the stomach, small
intestine, colon, pancreas, and spleen flows into two
large veins, the superior mesenteric vein and the
splenic vein, which unite to form the portal vein
• The portal vein takes blood into the liver, where it
branches extensively and empties blood into the
sinusoids, the capillaries of the liver
• From the sinusoids, blood flows into hepatic veins, to
the inferior vena cava and back to the right atrium
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Portal circulation---
Purpose
The liver stores some nutrients or regulates their blood
levels and detoxifies potential poisons before blood
enters the rest of peripheral circulation
Ex. Liver sinusoids, and the liver cells remove the excess
glucose and store it as glycogen. so that there is no
loss of glucose via urine
Ex. Alcohol is absorbed into the capillaries of the
stomach. If it were to circulate directly throughout
the body, the alcohol would rapidly impair the
functioning of the brain. Liver detoxify the alcohol
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Portal circulation
GI organs capillaries Large veins
Superior mesenteric Splenic vein
Unit & form Portal vein
Carries b/d to the liver sinusoids
Hepatic vein
Inferior vena cava
Right atrium
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Hepatitis
Def: - It is an inflammation of the liver
Liver span: 6-12 cm in the right midclavicular line
4-8 cm in the midsternal line (percusion)
Pathophysiology
Hepatocytes are damaged & become inflamed &
necrotised by the body's immune response to the
virus.
The degree of functional impairment depends on the
amount of hepato-cellular damage.
The hepatocytes generally heal in 3 to 4 months
Causes
- Virus , Bacteria , Toxic substances
Wollo University

Hepatitis type A /infectious hepatitis/
It is endemic in some areas of the world, especially with
poor sanitation
Causative agent: Infectious hepatitis virus(RNA)
Mode of transmission:
• Faecal – oral route (contaminated food, milk,
polluted water)
– Spread of the disease is enhanced by over-crowding &
poor sanitation
Incubation: - 15-45 days
Occurrence
• Worldwide – sporadic or epidemic
• Usually in children & young adults
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Hepatitis type A
C/M
1. Pre-icteric / pre-Jaundice/ phase 1-2days
- Headache - Pain over the liver , arthralgia
- Abdominal tenderness, - dislike of proteins
- Fever - Muscle cramp - Anorexia - Vomiting -
Backache - Nausea - Low grade fever
2. Icteric/ Jaundice/ phase
• Urine-dark; stool often light for several days b/se of
bilirubin
• Liver-enlarged, often tender
• Nausea, vague Epigastric distress, heart burn,
flatulence, anorexia
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Hepatitis type A---
Normal range
• ALT(SGPT)= 10- 40 u/L
• AST(SGOT) = 5-40 u/L Increases with
hepatitis
• ALP = 20 -147 Iu/L
• WBC = Increases
• Direct bilirubin (Conjugated) (N = 0.1 – 0.4 mg/dl)
• Indirect bilirubin (Unconjugated) (N = 0.2- 0.7 mg/dl)
• Bilirubun total ( N = 0.2-1.4 mg/L)
Bilirubin indirect = Bilirubin total – Direct bilirubin
• GGT (N =1- 94 u/L)
ALT > AST = Liver disease
AST > ALT (3:1,or 2:1) = Alcohol induced liver disease
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Hepatitis type A---
MGT
• Rest
• Vitamin B, C, & K
• Diet: Increase CHO, decrease protein & fat
• Drinking bottled water and avoiding fruits, vegetables, and raw
shellfish harvested from sewage-contaminated water
• Proper hygiene measures (frequent hand washing with soap and
water after using the bathroom and prior to eating meals)
• Proper disposal of sanitary waste
• Passive immunization with ISG ( two IM injections 6 months
apart (Immune serum globulin with in 2wks of exposure)
• Avoid alcohol
• Isolation (no carrier state with Hep A)
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Hepatitis B
Causative agent: - Hepatitis B Virus (DNA)
Mode of transmissions
A/ Parentral route
– Blood transfusion from an infected person (seminal & vaginal secretions)
– Contaminated needles, syringes
B/ Skin puncture – medical equipments
C/ Mucosal transmission; dental instruments ,saliva
Incubation period: 28-180 days
Occurrence: - world wide,10 % recovered cases are carriers
Diagnosis: - Count electrophoresis (CEP)
- Sandwich” Count electrophoresis (SCEP) - Radioimmunoassay
• IgM indicates active infection and anti-HBc to IgG relates to either chronic
infection or possible immunity against HBV.
C/M – S/S similar to infections hepatitis, but usually more insidious in onset
- Respiratory manifestations minimal or absent
- Increased risk of cancer
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Hepatitis B---
Rx & nursing Mx
• Isolate patient to minimize contacts
• Wear gloves; wash hands thoroughly
• Assist with laboratory diagnostic studies
• Handle bed pan carefully & instruct pt. to ensure
meticulous personal hygiene habit.
• Use disposable syringe & needles
• Avoid alcohol consumption
• Recognize that recovery is slow & prolonged
• Screen blood donors
• Passive immunization with ISG -Immune serum globulin
( needle stick exposure, mm, etc)
• Active immunization with Hep B for high risk
population( Ex. HW) at 1day, 30 day, & 6months
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Liver cirrhosis
Def
 It is a chronic disease in which there has been diffuse
destruction of parenchymal cells followed by liver cell
regeneration & an increase in connective tissue
• Cirrhosis is a chronic disease characterized by replacement
of normal liver tissue with diffuse fibrosis that disrupts the
structure and function of the liver
Def
Extensive scarring /chronic reaction to inflammation/ over a
long period
- There is scarring & permanent injury
- Chronic hepatitis & abnormal nodules
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Liver cirrhosis---
Classification
A/ Alcoholic cirrhosis of the liver (micro-nodular)
– Fibrosis – mainly around central veins & portal area
– Most commonly due to chronic alcoholism
B/ Post necrotic (Macro-nodular) –scar after hepatitis
• Due to previous acute viral hepatitis or drug induced massive
hepatic necrosis
C/ Biliary
• Scarring around bile ducts & lobes of liver
• Result from chronic biliary obstruction (with or without
infection)
• Much more rare than alcoholic & post necrotic cirrhosis
D/ Post hepatic
• Fine bands of scar tissue extend from portal areas
• Usually due to chronic viral hepatitis
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Liver cirrhosis---
Causes
• Alcohol abuse:- Facilitate scarring & fibrosis
• Hepatic fibrosis (Steato-hepatitis)
• Hepatitis virus (B & C)
• Drugs
* Methyldopa * Methotrexate * Toxins, etc
• Autoimmune chronic active hepatitis
• Excessive use of herbal medications
• Chronic hepatic congestion
• Bile duct obstruction
• Bile stasis
• Right sided heart failure
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Liver cirrhosis---
C/F
• Weight loss, muscle wastage, fatigue (65%)
• Flatulence - Jaundice, loss of body hair, gynacomastia
• Oedema , Bleeding - Anaemia 20 to bleeding
• Ascites , Hepatomegally + Spleenomegally
• Oesophageal varices
• Sign of hepatic encephalopathy
Diagnosis
• HX,P/E, Lab findings
• Decrease CBC, WBc, & plateletes
• Increase serum ammonia (N = 20-70 µgm/dl)
• Liver biopsy & liver function tests
• Esophagoscopy
• Liver scan
• Paracentesis to examine ascetic fluid
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Liver cirrhosis---
P/E
1/ Neurological
• Hepatic encephalopathy
• Peripheral neuropathy
• Peripheral oedema
• Asterixia = Liver flapping tremor(wrist & fingers)
2/ GI (Gastro-intestine)
• Nausea & vomiting , Hematemesis
• Anorexia
• Dyspepsia
• Change in bowel habit
• Dull abdominal pain
• Oesophageal/ gastric varices
• Haemorrhoids
• Congestive gastritis
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Liver cirrhosis---
P/E---
3/ Integumentary
Jaundice, Spider angioma, Palmar erythema ,Purpura &
petechiae ,Caput medusa, edema
4/ Haematological
Anaemia ,thrombocytopenia, coagulation disorder,
spleenomegally , fector hepaticus
5/ Metabolic
Potassium deficiency,hyponatremia & hypoalbuminemia
6/Reproduction
- Amenorrhea ,testicular atrophy ,impotency ,gynacomastia
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Liver cirrhosis---
Nursing management
A/ Nutrition
• Maintain caloric & vitamin diet
• Decrease protein & fat
• Avoid table salt, salty foods & canned foods
• Use ‘Salt’ substitutes such as lemon juice
• Offer small frequent meals
• Eliminate alcohol
• Restrict fluids
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Liver cirrhosis---
Nursing Management
B/ Medication
• Multivitamins preparation
• Vitamin K – if a tendency of bleeding is manifested such as
epistaxis, Melena, hematoemesis
• Vitamin B12 – to correct anaemia
• Diuretics e.g.: - Spirinolactone 100mg
• Maintain electrolyte & fluid balance
• Avoid toxic drugs:- Barbiturates, diazepam, methyldopa,
methotrexate, Oral contraceptive & Alcohol
• Cemetidine to decrease stress ulcer
• Neomycin and metronidazole to remove intestinal bacteria
which produces ammonia
• Lactulose 15-30 ml By: Wondwossen Yimam (Msc.N)
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Liver cirrhosis---
C/ Rest & activity
If there is no ascites & sign of hepatic coma: -
• Limit amount of activity
In advanced liver impairment
• Bed rest & elevate head to 30 0
• Frequent change of position
• Special skin care & passive exercise
• Observe for sign of bleeding
• Obtain consent for liver biopsy
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Liver cirrhosis---
Complications
• Hepatic coma
• Bleeding & oesophageal varies
• Portal hypertension
• Spontaneous peritonitis
• Ascites
• Anaemia
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Hepatic encephalopathy & hepatic coma
- Results from the accumulation of ammonia & other
toxic metabolites in the blood
The increased ammonia concentration in the blood
causes brain dysfunction & damage, resulting in
hepatic encephalopathy
• Hepatic coma
- Represents the most advanced stage of hepatic
encephalopathy
• Damaged liver cells fail to detoxify & convert ammonia to
urea, the ammonia that is constantly entering the blood
stream as a result of its absorption from the GIT & its
liberation from kidney muscle cells
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Hepatic encephalopathy & hepatic coma---
C/Ms
Early stage
Euphoria Depression
Apathy Irritability
Memory loss Confusion
Late stage
* Drowsiness * Insomnia
* Agitation * Slow & slurred speech
* Hyperactive reflex * Slow deep respiration
Impending coma
- Asterixa (Flapping tremor of hands)
- Fetor hepaticus
- Disorientation to PPT
Wollo University

Hepatic encephalopathy & hepatic coma---
Management
• Vital signs every 4 hours
• Daily monitoring of serum ammonia
• Diet:- Low protein & fat, High CHO
• Diet :- Vit B, C,& K
• Avoid constipation
• Enema to reduce ammonia absorption
• Sterilization of intestine (with neomycin sulphate &
metronidazole)
• Lactulose 15-30 ml po to reduce blood ammonia
Wollo University

Liver abscess
Def: - Formation of pus in the liver
Two categories of liver abscess have been identified
1.Amoebic liver abscesses: - most common
Cause: - Entamoeba histolytica
2. Pyogenic liver abscess
Less common
Cause: Staphylococcus, Streptococcus, E. Coli
Mechanism - GI infection
- Liver
- Abscess cavity formation
Wollo University

Unit V. Gastrointestinal disorders.pptx

Unit V. Gastrointestinal disorders.pptx

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