2. General objective
• After completion of this course, the student
will be able to assess, diagnose and manage
patients with medical surgical disorders
related to GIT , GUT and musculoskeletal
disorders and / or refer those requiring higher
level of management.
3. Contents
• Unit 1: Gastrointestinal tract (GIT) disorders
• Unit 2: Genito urinary tract (GUT) disorders
• Unit 3: Musculoskeletal system disorders
4. .
References:
1) Donna D. IGNATAVICIUS. A Nursing Process
approach Medical surgical
2) Medical surgical Brunner 11th Edition
3) Lackman and Sorensson medical surgical
nursing
4) Sharon medical surgical Nursing
5) Harrison’s principle of internal Medicine 16th
edition
6. Anatomy and physiology
• The GIT tract is pathway (23-to-26 feet or 7-8
meter in length) that extends from the mouth
through the esophagus, stomach and
intestines to the anus.
• It also includes organs that lie out side the
digestive tract i.e. pancreas, liver and gall
bladder.
6
7. Mouth and related structures'
• Digestion normally begins in the mouth,
Mouth and related structures includes
• Mucus membranes of the mouth
• Teeth
• Gums
• Lips
• Soft and hard plates
7
9. Cont---
Esophagus: is located in the mediastinum in
the thoracic cavity anterior to the spine and
posterior to the trachea and heart.
• Length: 23-25 cm (10 inch).
• At the upper end of the esophagus there is a
sphincter i.e. upper esophageal sphincter.
9
14. Cont---
• The inlet of the stomach is called the
esophagogastric junction.
• In the inlet there is lower esophageal
sphincter (or cardiac sphincter).
• In the out let: pyloric sphincter.
14
15. Cont---
Small intestine : is the longest segment of
the GI tract accounting for about 2/3 of the
total length
• Length: 5-6meters (16-19 feet)
• It is divided in to three anatomic parts
• The upper part, called the duodenum,
• The middle part called the jejunum and
• The lower part called the ileum.
15
17. Cont---
Cecum: is found in junction between the
small and large intestine.
• Is located in the right lower portion of the
abdomen.
• The ileocecal value is located at this junction.
• The vermiform appendix is located near this
junction.
17
18. Cont---
The terminal portion of the large intestine
consists of two parts
• The sigmoid colon and the rectum
• The rectum is continuous with the anus.
18
20. Function of the Digestive system
– To breakdown food particles in to the molecular
form for digestion
– To absorb the small molecules in to the blood
stream, produced by digestion
– To eliminate undigested and unabsorbed food
stuffs and other waste products from the body.
i.e. secretion, digestion, absorption, motility and
elimination.
20
21. Diagnostic test for common GIT
problems
I) Radiography:
• Is a simple x-ray without contrast agents.
• It shows obstruction or paralysis of the
digestive tract or abdominal air patterns in
the abdominal cavity .
• Also shows enlargements of organs like liver.
21
22. Cont---
II) Barium studies
• Entire GI tract can be out lined using a
contrast agent such as barium sulfate.
Barium swallow: ingested orally
Barium enema: instilled rectally
22
23. Cont---
III) Endoscopic procedures
• Examination of internal structures using a
viewing tube /endoscope.
• Many endoscopes have small scissors to
remove tissue sample and electric probe to
destroy abnormal tissue.
23
24. Cont---
A) Esophago gastro duodenoscopy (EGDS)
• Allows for direct visualization of esophageal, gastric,
and duodenal mucosa through a lighted endoscopy.
• Used for both diagnosis and treatment purpose.
• Pt NPO b/r and after the procedure.
• Local anesthetic sprayed is indicated.
• Position : left lateral.
24
26. Cont---
B) Laparoscopy
• Insert through the skin in the abdominal wall
under spinal or general anesthesia.
• Used to screen for tumor or other
abnormalities, to obtain sample, and to
examine any organ in the abdominal cavity
26
27. Cont---
C) Proctoscopy and sigmoidoscopy
• used to inspect/examine the rectum and
sigmoid colon respectively for the evidence
of ulceration, tumors, polyps, and other
abnormalities
D) Colonoscopy
• Examine the colon to the cecum
27
30. Cont---
IV) Gastric analysis
• Small tube into the stomach to obtain a fluid
sample.
• Stomach contents are aspirated by suction
into the syringe
• May be performed to diagnose gastric CA
30
31. Cont---
V) Stool examination
• Inspected for color, and consistency.
• If blood is lost large amount in the upper GIT
blood produce a tary black color/ Melena.
• If blood entering the lower portion of GIT
(passing rapidly through) it will appear bright
or dark red.
31
32. Cont---
• If there is streaking of blood on the surface of
the stool or if blood is noted on the toilet i.e.
lower rectal or anal bleeding is suspected.
• N.B. fecal occult blood test (FOBT) is a
common stool test to detect for CA(GI
bleeding associated with colorectal cancer)
32
33. Assessment
Health history and clinical manifestations
• The nurse begins by taking a complete history,
focusing on symptoms common to GI
dysfunction
33
34. Cont---
symptoms include: -
Pain - can be major symptoms
- Notify - the character
- location
- Duration
- Frequency
- Time of the pain
- Underline cause
34
36. Cont---
• Indigestion - due to disturbed nerves control of the
stomach
• Intestinal “Gas" (Belching and flatulence)
• Accumulation of gas in GIT may result belching
• Vomiting
• Hematemesis - vomiting of blood : bright red or
coffee ground appearance
36
37. Cont---
• Diarrhea - abnormal in stool liquidity
• Constipation - difficult defecation.
Physical assessment
• The Physical examination includes
assessment of the mouth, abdomen and
rectum.
• Inspection ---- auscultation --- percussion ----
palpation.
37
39. Problems of oral related structures
• Adequate nutrition is related to good dental
health and the general condition of the mouth,
because digestion normally begins in the
mouth.
• Changes in the oral cavity may influence the
type and amount of food ingested as well as
the degree to which food particles are
properly mixed with salivary enzymes.
39
41. A) Oral candidiasis /Trush
• Cheesy white plaque that looks like milk curds
w/n rubbed off it leaves erythematous and
often bleeding base.
• Is caused by fungus.
• Candida albicans is the most common agents
of candidiasis.
• Is the common form of candidiasis
41
42. Predisposing factors
Poor oral hygiene
Chronic illness like DM, HIV
Immunosuppressive therapy e.g. radiation
steroid therapy
Long term antibiotic therapy.
42
47. B) Leukoplakia
Chronic inflammation with thick patches on
mucous membrane.
Slowly developing changes in the oral
mucosa membrane that are characterized by
thickened white, firmly attached patches.
47
48. Cont---
• White patches usually on the tongue, gums,
and inside of checks.
• 90% of leukoplakia lesions are benign,
however, up to 7% of lesions becomes
malignant after many years.
• Lesions on the lips and tongue are more likely
to progress to malignancy
48
51. Causes
• Chronic irritation of the mouth (e.g. poorly
fitting dentures, broken or poorly repaired
teeth)
• Smoking, infected teeth.
• Very spicy foods
• Immunosuppressant e.g. HIV
• N.B. it can confused with oral Candidal
infection however, leukoplakia can’t removed
by scraping.
51
52. Cont---
• Hairy" leukoplakia of the mouth is an unusual
form of leukoplakia that is seen mostly in HIV-
positive people.
• It may be one of the first signs of HIV
infection.
52
54. Symptoms
• The most common symptoms of hairy
leukoplakia are painless, fuzzy /hairy white
patches on the side of the tongue.
• The skin lesions tend to have the following
characteristics:
• Location
– Usually on the tongue
– May be on the inside of the cheeks
54
55. Cont---
• Color
– Usually white or gray
– May be red (called erythroplakia, a condition that
can lead to cancer)
• Texture
– Thick
– Slightly raised
– Hardened surface
55
56. Management
• Removing the source of irritation is important and
may cause the lesion to disappear.
• Treat dental causes such as rough teeth, irregular
denture surface, etc
• Stop smoking and do not drink alcohol.
• Some times surgery may require to remove the
lesion.
56
57. Prognosis
• Lesions often clear up in a few weeks or
months after the source of irritation is
removed.
57
58. C) Stomatitis
• Is also called canker sore
• Shallow ulcer with a white center and red border
• The sore usually forms on the soft, loose tissues
particularly on the inside of the lips or cheek,
tongue, soft palate and sometimes in the throat.
• It is very common (affecting 20% of the general
population to some degree)
• Episode occurs 3-6 times per year
58
60. Possible causes
Vitamin deficiency (B-
complex, folic acids,
Zink, iron)
infection (bacterial, viral
or fungus)
systemic diseases (HIV,
DM, leukemia)
irritants ( tobacco, and
alcohol)
Chemotherapy or
radiation therapy.
allergies, acidic foods
it is also associated
with emotional or
mental stress,
fatigue, or hormonal
factors and genetic
predisposition
60
61. Sign and symptoms
• No detectable systemic
symptoms of or signs
out side the mouth
• pain lasts 4-10 days
• Fever and dry mouth
• Shallow ulcer with or
gray center and red
border.
• It begins with burning,
itiching or tingling
sensation and slight
swelling
• Tongue may be dry,
cracked, contain masses
or exudates.
• Sensitivity to hot and
spicy foods.
• Oral bleeding
61
62. Mgt
• Control or remove
causes
– Improve diet
– Rx treatment of
underlying infections
with Abs.
• Good oral hygiene
Medications
• Analgesics for pain,
• Topical/systemic
steroids
62
63. Cont---
Antimicrobials (to treat as well as to prevent
secondary infection)
• Abs
E .g. TTC syrup 250/10ml QID for 10 days.
• Antiviral:
IV acyclovir (infused at constant rate over a
1hr period every 8hrs for 7days
• Antifungal
• Rest: to promote tissue repair 63
64. Reading assignment
Disorders of teeth gums & salivary gland
–Gingivitis
–Dental plaque and caries/cavities
–Periapical abscess
–Parotits
–Oral cancer
64
65. Esophageal disorders
There are many pathologic conditions of the
esophagus, including:
• Esophagitis
• Motility disorders
• Hiatal hernias, and
• Diverticula,
65
66. A) Esophagitis
• Is an acute or chronic inflammation of the
esophagus.
• It also called gastro esophageal Reflux disease
(GERD).
66
67. Causes
• Gastro esophageal
reflux
– Inappropriate relaxation
of LES.
– Delayed gastric emptying
– Medication that reduces
strength of LES (like OCP,
nitrates, sedatives, B-
blockers, calcium
channel blockers and
anticholinergics)
• Trauma
– Swallowing of foreign
bodies
– Prolonged Naso - gastric
intubation
– Repeated vomiting
• Infection
• Chemicals: acids, alkalis
67
68. C/M
• Dyspepsia/indigestion
• Heart burn
• A sensation of acidic or
bitter regurgitation
associated with nausea
• Bleeding (acute or
chronic
Dysphagia or
odynophagia (pain on
swallowing)
Pain on
drinking/alcohol, hot or
cold fluid
Worsen w/n the client
bends over, strain, or in
recumbent position.
68
70. Management
• Depends on the cause of esophagitis
1) life style changes
– The patient is instructed to eat slowly and chew
foods thoroughly (to avoid belching )
– avoid caffeine, beer /alcohol and smoking,
– Avoid acidic foods e.g. orange juice, tomatoes etc.
– Raising the head of the bed /15-20cm
70
71. Cont---
- Remain upright 1-2hrs after meal
- No food or drink with in 2-3hrs of bed time
- Avoid lifting of heavy objects or straining and
working in bent over position.
- Avoid heavy meal / Eat a low-fat diet
- Encourage small and frequent diet 4-6 times
than large foods 3 times /day
- N.B. left lateral position reduces GER!
71
72. Cont---
2) Chemotherapy
• Antacids after each meal and before bed time.
• Accelerate gastric emptying e.g.
metoclopramide /prokinetic drugs
• Anti secretory agents
• Antibiotics if associated with infection
72
73. 2) Achalasia
• Is a motility disorder.
• Is absent or ineffective peristalsis of the distal
esophagus accompanied by failure of the
esophageal sphincter to relax in response to
swallowing.
73
74. Cont---
• Narrowing of the esophagus just above the
stomach results in gradually increasing
dilation of the esophagus in the upper chest.
• The exact cause is unknown
74
76. c/m
• Difficulty in swallowing ( both liquid and
solid): The 1st symptom
• Sensation of food sticking in the lower portion
• Food is commonly regurgitated,
• May have chest pain and heart burn
• Halitosis (unpleasant-smelling breath)
• Pain may or may not be associated with eating
76
77. Diagnostic Evaluation
• Radiological studies - show esophageal
dilation above the narrowing at the gastro
esophageal junction
• Barium swallow and endoscopy may be used
to diagnosis.
• c/ms
77
78. Management
• Patient should be instructed to eat slowly and
to drink fluids with meals and avoid foods that
aggravate the condition.
• Mild cases can be treated with Ca++ channel
blockers and nitrates have been used to
decrease lower esophageal pressure and
improve swallowing.
78
79. Cont---
• If this is unsuccessful
• pneumatic (forceful) dilation: by passing a
tube into the esophagus i.e. large metal stents
maybe used to keep esophagus open for
longer duration.
• Has 75% success rate and a 3% incidence of
perforation
79
83. C) Esophageal Diverticula /pouches
• Diverticulum: is an out pouching of mucosa
and sub mucosa that protrudes through a
weak portion of the musculature.
• Esophageal diverticula: is a sacs resulting
from the herniation of esophageal mucosa
and sub mucosa into the surrounding tissue.
83
84. Cont---
It may occur in one of the three areas of the
esophagus:-
• The pharyngo - esophageal or upper area of
the esophagus (most common)
• The mid esophageal area or
• Epiphrenic or lower area of the esophagus
84
87. C/M
• Difficulty swallowing
• Fullness in the neck
(feeling that food stops
before reaching in to
the stomach)
• Belching
• Halitosis
• Regurgitation of
undigested foods
• Diverticulum /pouch
filled with food or fluid
87
89. Management
• The only means of cure is surgical removal of
the diverticulum /diverticullectomy
• After surgery foods and fluids are withheld
until x-ray is confirm no leakage at surgical
site.
89
90. Gastric and duodenal disorders
A) Gastritis
Inflammation of the gastric or stomach
mucosa
it is a common GI problem.
It may be acute, lasting several hours to few
days, or chronic , resulting from repeated
exposure to irritating agents or recurring
episodes of acute gastritis.
90
91. Cont---
Acute gastritis : inflammation of the gastric
mucosa after exposure to local irritants.
Causes:
• is often caused by dietary indiscretion.
• The person eats too much or too rapidly or
eats food that is contaminated or too highly
seasoned or is infected.
91
92. Cont---
• Other cause includes – alcohol, aspirin, bile
reflux, or radiation , infection (staph, strep, E.
coli, salmonella. )
• More severe form of acute gastritis is caused
by ingestion of strong acids or alkalis
• Gastritis also may be the 1st sign of an acute
systemic infection
92
93. Cont---
C/M - Acute gastritis
• Rapid onset of gastric
pain or discomfort
• Dyspepsia /heart burn
• Abdominal discomfort
• Headache
• Nausea, anorexia
• Vomiting /
hematemesis
• Some patients,
however, are
asymptomatic.
93
94. Cont---
Chronic gastritis
– Prolonged inflammation of the stomach may be
caused by either benign or malignant ulcers of the
stomach or by the bacteria helicobacter pylori.
– Appears as a patchy diffuse/spread out
inflammation of the mucosal lining of the
stomach.
94
95. Cont---
• it may also be associated with dietary factors such as
hot drinks or spices, use of drugs, alcohol, smoking
or reflux of intestinal contents in to the stomach.
95
96. Cont---
C/ms of chronic gastritis.
• Heartburn/ epigastric pain
• Anorexia
• Belching
• Sour taste in the mouth
• Vomiting and nausea
• Pernicious anemia
96
98. Management
• The gastric mucosa is capable of repairing itself after
a bout of gastritis
• Avoid foods /drinks that cause distress coffee, tea
,chocolate, alcohol and smoking
• Instruct the patient to refrain from alcohol and food
until symptoms subside.
• Encourage nonirritating diet
• Bed rest
98
99. Cont---
for Chronic gastritis
• is managed by modifying the patient’s diet
• promoting rest,
• reducing stress and
• initiating pharmacotherapy (antacids,
sucralfate, and Abs)
99
100. Nursing intervention
• Assess and document signs and symptoms and
reactions to treatments
• Monitor intake and out put.
• Provide the prescribed diet.
• Administer medication as prescribed and monitor for
side effects.
• Note amount and character of emesis and diarrhea
and Monitor IV fluids.
• Educate patient and family concerning drug therapy,
diet activities and any restrictions.
100
101. B) Peptic ulcer diseases (PUD)
• A peptic ulcer is an excavation (hollowed-out area)
that forms in the mucosal wall of the stomach, in the
pylorus (opening between stomach and duodenum)
in the duodenum or in the esophagus.
• It is frequently referred to as gastric, duodenal or
esophageal ulcer, depending on its location or as a
peptic ulcer disease.(PUD)
101
103. Cont---
• Erosion of a circumscribed area of mucus
membrane is occurred.
• This erosion may extend as deeply as the
muscle layers or through the muscle to the
peritoneum
• Peptic ulcers are more likely to be in the
duodenum than in the stomach,
103
106. Cont---
Incidence:
• Has greater frequency occurrence b/n ages of
40 and to 60 hrs
• Relatively uncommon in women child bearing
ages i.e. man to women ratio 3:1
• Man to women ratio after menopause 1:1
106
107. Cont---
Causes:
• Increase secretion of Hcl and pepsin acid or
• Decrease in the normal resistance of the
mucosa.
• Gram-negative bacteria H. pylori
107
108. Cont---
Predisposing factors
• Stress (occupational stress ,and emotionally stress
• Emotional tense persons/anger
• Hereditary link persons with Blood group O are 35%
more susceptible than others
• Other predisposing factors associated with peptic
ulcer include caffeine, smoking, alcohol ingestion,
chronic use of NSAIDS
108
109. Pathophysiology
• The erosion is due to an increase in
concentration or activity of acid – pepsin or
due to a decrease in the normal resistance of
the mucosa.
• A damaged mucosa is unable to secrete
enough mucus to act as a barrier against HCl
acid.
109
110. Cont----
• When a break in mucosal barrier; the Hcl
injuries the epithelium.
• Rapidly emptying of food from stomach
reduces the buffering effects of food and
delivers a large acid bolus to the duodenum
leading to duodenal ulcer.
110
111. Clinical manifestation
• Symptoms ulcer may last for a few days,
weeks, months may even not disappear.
• Dyspepsia/ indigestion: discomfort centered
around the epigastrium or upper abdomen is
the most common reported symptoms
111
112. Cont---
• Pain – dull, gnawing(cramp) pain, or a burning
sensation in the mid epigatrium or in the back.
• It is believed that pain occurs w/n there is increased
acid content of the stomach and duodenum.
• Sharply localized tenderness can be elicited by
applying gentle pressure to the epigastrium or
slightly to the right of the midline.
• Some relief is obtained by applying local pressure on
the epigastrum.
112
113. Cont---
• Pyrosis(heart burn): some patients experience
a burning sensation in the esophagus and
stomach.
• Vomiting : is rare in uncomplicated duodenal
ulcers.
• Constipation and bleeding: perforation or
hemorrhage may occur with any preceding
manifestations.
• Abdominal distention/fullness.
113
114. Comparing Duodenal and Gastric Ulcer
Duodenal Ulcer/DU
Incidence
• Age 30-60
• Take 80%
• hyper secretion of HCL
Gastric Ulcer/GU
• Usually 50 and above
• 15% of cases
• Normal-hypo secretion
of HCL
114
115. DU GU
• Pain occurs after 2-3hrs
of a meal
• Ingestion of food relives
pain
• May have wt gain
• Vomiting uncommon
• Pain occurs ½ to 1hr
after a meal ;may
relived by vomiting
• Ingestion doesn’t help,
sometimes it may
increase pain;
• Weight loss may occur
• Vomiting common
115
116. DU GU
• Hemorrhage less likely
than with G.U
• But if present, melena
is more common than
hematemesis
• More likely to perforate
than G.U
• Malignancy : rare
• Hemorrhage more likely
to occur than with
duodenal ulcer;
• Hematemesis more
common than melena
• less likely to perforate
• Malignancy:occasionally
116
117. Diagnostic Evaluation
• History and physical examination/bowel
sound may be absent
• C/ms: Pain relived by ingesting food or
antacids – suggestive of duodenal ulcer.
• Barium study of the upper GI tract may show
an ulcer - X-ray
117
118. Diagnosis Cont---
• Endoscopy: is the preferred diagnostic procedure to
detect those lesions not evident in x ray studies b/c
of the size and location of lesions.
• Stool- for occult blood
• Gastric secretion studies
• Serologic test for antibodies of H.pylori Ag.
118
119. Management of PUD
A) Nondrug management
• Stress reduction and rest
• Smoking cessation
Dietary modification: avoid foods that
increase secretion of acid e.g. coffee, alcohol,
cola, cram, milk,
119
120. Cont---
• Small and frequent foods
• Food it self acts as an antacid by neutralizing
gastric acid for 30-60 minutes then an
increased gastric secretion follows.
• Follow up care
120
121. Cont---
B) Drug mgt
I) Antacids
• Magnesium hydroxide and or Aluminum
hydroxide 50-80 MEq 1hr and 3 hr after meal
and at bed time.
121
122. Cont---
II) H2 Receptors antagonist
• Cimetidine : 300mg PO Qid for 4-6 week (400mg
BID and 800 mg once)
• Ranitidine : 150 mg PO BID for 4-6 week (300mg PO
at bed time)
• Famotidine : 40 mg po once a day for 4-6 week
• Nizatidine : 150 mg PO BID or 300mg at bed time.
122
123. Cont---
III) Antisecrotary agents
• Omeprazole 20mg PO BID or 40mg at bed time
• Lansoprazole 15 or 30 mg PO at bed time.
• Panto prazole 40mg PO IV daily
• Esomeprazole 20mg or 40 mg PO daily.
IV) Mucosal barrier fortifiers
• Sucralfate 1gm PO QID or 2gm twice daily.
123
125. Cont---
PUD associated with H. pylori
• First line: Amoxicillin 1gm PO BID +
clarithromycin 500 mg PO BID + omeprazole
20mg PO BID or 40mg once daily.
• Alternative: amoxicillin + metrindazole 500mg
PO BID + omeprazole
125
126. Cont---
C) Surgical management
• Surgical intervention for peptic ulcers is less
common
• It usually recommended for patient with
intractable ulcers, life threatening
hemorrhage, perforation, obstruction
126
127. Cont---
It includes:
A) Vagotomy: Severing of the vagus nerve.
Decreases gastric acid by diminishing
cholinergic stimulation to the parietal cells,
making them less responsive to gastrin.
reduce gastric acid secretion
127
129. Cont---
B) Billroth I : antrectomy with anastmosis to the
duodenum / gastro- duodenostomy
• Removal of the lower portion of 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 (Billroth I)
129
131. Cont---
c) Billroth II: antrectomy with anastmosis to the
jejunum /gastro- jejunostomy.
• Removal of distal third of stomach;
anastomosis with jejunum.
• Removes gastrin -producing cells in the
antrum and part of the parietal cells
131
133. Cont---
• Potential complications
– Hemorrhage
– Perforation
– Pyloric obstruction (it occurs when the area distal
to the pyloric sphincter becomes scarred and
stenosed from spasm or edema)
– Intractable ulcers (hard to control)
133
134. C) Gastric Cancer
• Mostly occurs in people over age of 40 and
occasionally in younger people.
• Most stomach cancers occur in the lesser
curvature , pylorus or antrum of the stomach
and are adenocarcinomas
• The tumor infiltrates the surrounding mucosa,
penetrating the wall of the stomach &
adjacent organs and structures
134
135. Cont---
• The liver, pancreas, esophagus and duodenum are
often affected at the time of diagnosis.
• Diet appears to be a significant factor. i.e. a diet high
in smoked foods and low in fruits & vegetables may
increase the risk of gastric cancer.
• Other factors related to the incidence of gastric Ca
include chronic inflammation of the stomach,
pernicious anemia, achlohydria, gastric ulcers, H.
pylori infection and genetics.
135
137. Cont---
C/M
• In the early stage of gastric Ca symptoms may
be absent.
Symptoms of progressive disease may include:
• anorexia( lack of appetite), dyspepsia,
(indigestion), wgt loss, abdominal pain,
constipation, anemia & N/V.
137
138. Cont---
Diagnostic Evaluation
• P/E is usually not help full, as most gastric
tumors are not palpable
• X-ray with barium swallows.
• Endoscope for Biopsy and cytological study
• Computed tomography (CT) scan
138
139. Cont---
Management
• There is no successful Rx of gastric carcinoma
except removal of the tumor.
• If the tumor can be removed while it is still
localized to the stomach, the patient can be
cured.
• If the tumor has spread beyond the area –cure
cannot be effective
139
140. Cont---
Surgical mgt
• Radical subtotal gastrectomy - the stump of
the stomach is anastomosed to the Jejunum
• Total gastrectomy – GI continuity is restored
by an anastomoiss b/n the ends of the
esophagus and jejunum.
140
142. Cont---
Nursing interventions
1) Preoperative care
• Support the patient and family
• Assess and document signs and symptoms and
reaction to treatments
• Provide and encourage the prescribed diet
• Monitor vital signs at least Q 8 hrs
• Monitor blood and fluid replacement therapy
• Provide preparative teaching
142
143. Cont---
2) Post operative care
• Have patient turn, cough and breathe deeply
• Monitor NG suctioning and tube patency
• Monitor vital signs as ordered
• Record intake and out put
• Administer prescribed medications and
monitor for side effects
143
144. Cont ---
• Encourage early ambulation and Rome (rapid
eye movement exercises to prevent
thrombosis
• Provide anti embolism and supportive
measures
• Analgesics if pain occurs, and supportive
measures
• Educate patient and family concerning drug
therapy dietary restrictions, activity,
144
145. Intestinal disorders
Intestinal Obstruction
• It exists when blockages prevents the normal
flow of intestinal contents through the
intestinal tract.
• Two types of process can impede flow:
1) Mechanical obstruction - an intraluminal
obstruction from pressure on the intestinal
walls.
145
146. Cont--
Mechanical obstruction can be caused by:
• Intussusceptions: one part of the intestine
slips in to the another part located below it
like a telescope shortening.
• Adhesions: loops of the intestine become
adherent to areas that heal slowly or scar
after abdominal surgery
146
147. Cont---
• Volvlus: bowel twist and turns upon it
• Hernias: protrusion of intestine through a
weakened area in the abdominal muscle or
wall.
• Tumors, and neoplasm
147
149. Cont---
2) Functional obstruction: the intestinal
musculature cannot propel the contents
along the bowel.
• E.g. muscular dystrophy, endocrine disorders
such as DM, or neurological disorders such as
Parkinson’s disease
149
150. Cont---
• The obstruction can be partial or complete.
• Its severity depends:
• On the region of bowel affected
• The degree to which lumen is occluded and
• Especially the degree to w/c vascular supply is
disturbed
150
151. A) Small bowel obstruction (SBO)
• Most bowel obstructions (85%) occur in the
small intestine, Adhesion is the most common
cause of SBO, followed by hernias and
neoplasms.
151
152. Cont----
Pathophysiology
• In SBO, intestinal contents, fluid, and gas accumulate
above the intestinal obstruction
• The abdominal distension and retention of fluid
reduce the absorption of fluids and Stimulate more
gastric secretion
• This caused edema, congestion, necrosis and
eventually rupture or perforation of the intestinal
wall, with resultant peritonitis.
152
153. Cont---
• Reflux vomiting may be caused by abdominal
distension
• Dehydration and acidosis develop from loss of
water and sodium.
• With acute fluid losses hypovolemic shock
may occur.
153
154. Cont---
C/M-
• Initially crampy pain that is wavelike and
colicky.
• blood and mucus may pass, but no fecal
matter and no flatus.
• Abdomen becomes distended
154
155. Cont---
• If obstruction is complete- the peristaltic wave
become reverse direction so intestinal content come
to the mouth
• If obstructions 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.
155
156. Cont---
Sign of DHN become evident i.e. intense thirst
• Drowsiness
• Generalized malaise
• abdominal distention
• hypovolemic shock from DHN and loss of plasma
volume and
• constipation
156
157. Cont---
Diagnostic Evaluation
• patient Hx and P/E
• X-ray findings (shows abnormal quantities of
gas, fluid or both in the bowel)
• Laboratory studies (electrolyte studies and
CBC)
157
158. Cont---
Management
• Decompression of the bowel through a
nasogastric tube is successful in most cases
• Complete obstruction needs , surgical
intervention /depends on the cause of
obstruction i.e.
– if adhesion dividing the adhesion to which
intestine is attached ,
– if hernia: repairing of hernia.
158
159. Cont---
• IV therapy to replace the depleted water, and
electrolyte before surgery
• prophylactic antibiotics
• monitor intake and out put
• supportive care
159
160. Cont---
Nursing intervention
• Maintaining the function of the NG tube
• Assessing and measuring the nasogastric out put
• Assessing for fluid and electrolyte imbalance
• prepare the pt’ for surgery
• Assess and document signs and symptoms and
relations to treatments
• Monitor V/S at least Q 4 hrs
• Record intake and out put
160
161. Cont---
• Administered prescribed medication and
monitor for side effects
• maintain NPO
• monitor the state of distention and hydrations
• provide routine post operative care if patient
undergoes surgery
161
162. B) Large bowel obstruction (LBO)
• About 15% of intestinal obstruction occur in
the large bowel and the most common cause
are carcinoma, diverticulitis, inflammatory
bowel diseases and benign tumors
• Most are found in sigmoid colon.
162
163. Cont----
• As in small bowel obstruction, large bowel
obstruction results in an accumulation of intestinal
contents, fluid and gas proximal to the obstruction.
• Even if the obstruction is complete, it may be
undramatic if the blood supply to the colon is not
disturbed.
• If the blood supply is cut off, however strangulation
and necrosis (i.e. tissue death) occur, this condition is
life threatening.
163
164. c/ms
• LBO differs clinically from small bowel
obstruction in that Symptoms develop slowly
relative to SBO
• Constipation (if obstruction in sigmoid colon
or the rectum).
• Abdomen becomes markedly distended
164
165. Cont---
• Loops of large bowel becomes visibly outlined
through the abdominal wall.
• Eventually, Crampy lower abdominal pain
• Dehydration occurs more slowly than in the
small intestine
165
166. Cont---
Diagnosis
• Based on symptoms
• X-ray studies (show distended colon)
• Barium enema is contraindicated.
166
167. Cont---
Management
• Colonoscopy may be performed to untwist
and decompress the bowel.
• Rectal tube to decompress.
• The usual Rx, however, is surgical resection to
remove the obstructing lesion.
167
168. Cont---
• Cecostomy /surgical opening of the cecum /
may be performed.
• Temporary or permanent colostomy may be
necessary /is the surgical creation of an
opening into the colon to drainage or
evacuation colon contents to the outside of
the body.
168
169. Acute inflammatory intestinal
disorders.
• Any part of the lower gastrointestinal tract is
susceptible to acute inflammation caused by
infection due to bacteria, virus, or fungus.
• The two sever situations are appendicitis and
diverticulitis. And others include peritonitis
and gastroenteritis.
169
170. A) Appendicitis
• Appendix is a small, finger like appendage about 10
cm long that is attached to the cecum just below the
ileocecal valve
• Has no definite function
• The appendix fills with food and empties regularly in
to the cecum
• Because it empties inefficiently and its lumen is
small, the appendix is prone to obstruction and is
particularly vulnerable to infection.
170
171. Cont---
• Appendicitis: It is an inflammation of the
appendix.
• Is the most common cause of acute
inflammation in the RLQ of abdominal cavity
• Is the most common reason for emergency
surgery.
• People consume a diet low in fiber and high in
refined carbohydrates are more liable
171
172. CAUSES OF APPENDICITIS
Traumatic injury to the abdomen
Feces blocks the inside of appendix
Genetics
Genetic variant that predisposes a person to
obstruction of the appendiceal lumen
173. CAUSES OF APPENDICITIS
Obstruction of the lumen by:
A fecalith (accumulated feces)
Foreign bodies
Worms (e.g., Pinworms, ascaris)
Intramural thickening caused by lymphoid hyperplasia
Tumors of the cecum or appendix
Kinking of appendix
Inflammation
Neoplasm
176. Cont---
C/M
• Right lower quadrant pain and is usually
accompanied by a low-grade fever and nausea
and vomiting sometimes
• Loss of appetite
• Local tenderness noted in Mcburaey’s point.
(Located ½ way b/n the umbilicus and the
anterior spine of the ileum)
176
179. Cont---
• If the appendix is has ruptured, the pain
becomes more diffuse.
• abdominal distention, develops as a result of
paralytic illus .
• Constipation can also occur
• In general, laxative or cathartic should never
be given while the person has fever nausea or
pain.
179
183. Psoas Sign: 2 methods
1st Method
Place your hand just above the patient’s right knee
Ask the patient to raise that thigh against your hand (extending right
thigh)
2nd Method
Ask the patient to turn onto the left side
Then extend the patient’s right leg at the hip
Flexion of the leg at the hip makes the psoas muscle contract;
extension stretches it 183
185. Rovsing’s sign
• Elicited by palpating the LLQ; this
paradoxically causes pain to be felt in the RLQ
185
186. Positive Obturator Sign
Flex the patient’s right thigh at the hip, with the knee bent,
and rotate the leg internally at the hip
This maneuver stretches the internal obturator muscle
If the appendix has ruptured
The pain becomes more diffuse
Abdominal distention develops
The patient’s condition worsens
186
191. Tzanakis Score
1. Rt lower abdominal tenderness = 4
2. Rebound tenderness = 3
3. WBC’s> 12,000 in the blood = 2
4. Positive USS findings of appendicitis = 6
• Total score = 15
• > 8 = 96% chances
192. Management
1) Supportive treatment
• Correct fluid and
electrolyte imbalance
and DHN.
• Antibiotics
• If surgery is undecided
avoid analgesic
2) Surgery: is indicated if
appendicitis is
diagnosed==>appendec
tomy.
192
193. Cont---
Complications
• The major complication of appendicitis is
perforation of the appendix, which can lead to
peritonitis or abscess.
• Incidence of perforation is 10-32%
• It generally occurs 24hrs after the onset of
pain. Symptoms include a fever of 37.7oC or
higher, and continued abdominal pain or
tenderness.
193
194. B) Peritonitis
• Peritoneum is the serous membrane lining the
abdominal cavity and covering the viscera.
• Peritonitis is an acute inflammation of the
peritoneum
• It can be classified as primary (as TB) and
secondary (secondary to trauma, bile leakage )
and localized and generalized.
194
195. Cont---
• It is commonly caused by the leakage of
contents from abdominal organs into the
abdominal cavity, and lead to contamination
of peritoneal cavity by bacteria usually as a
result of inflammation, infection, or trauma
195
196. Etiology
• Usually it is a result of bacterial infection, the
organism come from disease of the GI tract (
e. coli, streptococcus, staphylococcus, etc )
or, in women, from the internal reproductive
organs (Gonococcus).
• Bacteria gain entry into the peritoneum by
perforation or from external penetrating
wound.
196
197. Cont---
• The most common causes of bacteria
peritonitis are appendicitis, perforation
associated with PUD, diverticulitis, and bowel
obstruction.
• It can also result from external sources such as
injury or trauma (ex. Gunshot wound, stab
wound), or inflammation that extend from an
organ outside peritoneal area.
197
198. c/ms
• It depends on the location and extent of
inflammation
• The cardinal signs of peritonitis are
abdominal pain / tenderness localized or
generalized) and progressive abdominal
distention.
• At first, diffuse type of pain is felt
198
199. Cont---
• The pain tends to become constant, localized
and more intense near the site of
inflammation
• The affected area of the abdomen becomes
extremely tender and distended and the
muscles become rigid.
199
200. Cont---
others
• fever
• N/V/anorexia
• diminished bowel sounds
• inability to pass flatus and or feces
• pulse rate increase
• Dehydration
• Respiratory difficulty
200
201. Cont---
Diagnostic Evaluation
• c/ms
• lab, increase WBC(> 20,000/mm3)
• abdominal X-ray
• Peritoneal dialysis (positive for peritonitis if
more than 500 WBC/ml of fluid or more than
50,000 RBCs/ml of fluid or Presence of
bacteria )
201
202. Management
• Hospitalization
• Fluid, and electrolyte
replacement is the
major focus.
• Iv fluids
• Analgesics are
prescribed for pain
• Broad spectrum
antibiotics therapy
• NG tube is inserted to
decompress the
stomach and intestine
and the client is on NPO
status
• Oxygen if respiratory
distress.
202
203. Cont---
• Positioning: semi fowlers position to promote
drainage of peritoneal contents in to inferior
region and abdominal cavity and also to it
facilitate adequate respiration.
• Surgical if critically needed: exploratory
laparotomy ; to remove or repair the inflamed
or perforated organ;
203
204. Cont---
Complication
• Sepsis is the major cause of death from
peritonitis
• Shock – from septicemia or hypovolemia
• Intestinal obstruction – from inflammatory
process 10 from development of bowel
adhesions
204
205. C) Diverticulitis
• Diverticula are congenital or acquired pouch
like herniations of the mucosa through the
muscular wall of the small intestine or colon.
• Diverticula can occur in any part of the small
or large intestine but they occur most
commonly in the sigmoid colon.
205
206. Cont---
• Diverticulosis is the presence of many
diverticula without inflammation or
symptoms.
• Diverticulitis is the term used to describe an
inflammation of one or more diverticula,
206
207. Causes
• It forms when the mucosa and sub mucosal layer of
the colon herniated through the muscular wall
because of
• High intraluminal (abdominal) pressure and
• Decreased muscle strength in the colon wall
(i.e. muscular hypertrophy from hardened fecal
masses or w/n blood supply interrupt ).
• Chronic constipation precedes the
development of diverticulosis by many years
• Eating diet with small fiber can increased the
risk of diverticula. 207
208. Cont---
• Undigested foods or bacteria can become
trapped in the diverticulum = diverticulum
becomes inflamed and local abscess forms =
diverticulitis
• Abscess develops and may eventually
perforate, = leading to peritonitis
208
209. Cont---
C/M
• Bowel irregularity and intervals of diarrhea
• Abrupt onset of crampy pain in the LQ
• Fever
• V/N, anorexia and abdominal distension
• Bleeding
• If untreated, septicemia develop
209
211. Management
• Combination of drug and diet therapy with
rest to decrease inflammation and to
improve tissue perfusion.
• When symptoms occur, rest, analgesics and
antispasmodics are recommended
• Initially, the diet is clear liquid until the
inflammation subsides: then a high fiber, low-
fat diet is recommended.
211
212. Cont---
• Broad spectrum antibiotics e.g. metrindazole
+ Cotrimoxazole, anti pains and
anticholinergics (to reduce intestinal motility)
are recommended
• enema and laxatives are avoided = increase
intestinal motility
• encourage to avoid activities that increase
abdominal pressure e.g. straining, bending,
lifting etc
212
213. Cont---
• Surgical management :- immediate surgical
intervention is necessary if complications (Ex.
Perforation/rupture , abscess formation,
hemorrhage, peritonitis and bowel
obstruction)
213
214. D) Gastro enteritis
• Is an increase in the frequency and water
contents of stool or vomiting as result of the
inflammation of mucous membrane of the
intestinal tract and stomach
• It can be viral (e.g. rota virus) or bacterial ( e.g.
E.coli, shigellosis, ameobiasis,) in origin.
• Usually self limiting if no complication
214
215. Cont---
Mgt
• Treatment of the c/ms plus
• drug mgt depends on the lab result
• e.g. if bacterial Abs ( Norfloxacillin 400mg PO
BID, or ciprofloxacilin 500mg PO BID for
3days)
• If viral only supportive treatment (Rx of DHN,
antiemetic, anticholenergis to suppress
intestinal motility)
215
216. Chronic inflammatory Bowel Disease (IBD)
• Is disorders of the lower GIT, and it refers to
two chronic inflammatory GI disorders:-
–Ulcerative colitis
–Regional enteritis (crohn’s disease)
216
217. A) Ulcerative Colitis
• Is a recurrent ulcerative and inflammatory
disease of the mucosal and sub mucosal layers
of the colon and rectum with unknown
etiology.
• Sometimes following bowel infection,
Autoimmune (antibody against bowel
epithelium) can be a contributory factors
217
218. Cont---
• It affects the superficial mucosa of the colon
and is characterized by multiple ulcerations,
diffuse inflammations
• Bleeding occurs as a result of the ulcerations.
• The mucosa becomes edematous and
inflamed
• The disease process usually begins in the
rectum & spreads proximally to involve the
entire colon.
218
219. Cont---
• Is a serious disease accompanied by systemic
complication and high mortality rate.
• Eventually 10-15 % of the pt develop
carcinoma of the colon.
• Peak incidence 30-50yrs.
219
220. Cont---
C/M
• Diarrhea(10 to 20 times /day),
• LLQ abdominal pain,
• intermittent tensemus and rectal bleeding are
the predominant symptoms.
220
221. Cont---
Others: May have anorexia, wt loss, fever,
vomiting and dehydration, as well as
cramping, the feeling of an urgent need to
defecate .
• Hypocalcemia & anemia frequently develop.
• Rebound tenderness may occur in the right
lower quadrant (suggests peritonitis)
221
222. Cont---
Diagnostic evaluation
• Stool is +ve for blood
• Low Hgb and HCT and increases WBC
• X-ray (abdominal)
• Sigmodoscopy, or colonoscopy
• Stool examination for parasites and other
microbes (to rule out dysentery caused by
common intestinal organisms like
E.histolytica) 222
223. Management
Nutritional therapy
• Oral fluids,high protein, high-calories diet with
supplemental vitamin therapy and iron
replacement are prescribed to meet
nutritional needs, reduce inflammation, and
control pain and diarrhea
• Any foods that exacerbate diarrhea are
avoided ex. Milk, may contribute to diarrhea
in those with lactose intolerance.
223
224. Cont---
Pharmacologic therapy
• Antidiarrheal & anti peristaltic medications
are used to minimize peristalsis to rest the
inflamed bowel
• Aminosalicylate formulations are often
effective for mild or moderate inflammation
• Corticosteroids are used to treat severe
disease
224
225. Cont---
• Surgical management may recommend when
medical measurement fail to relive the severe
symptoms.
• e.g. total proctocolectomy /colectomy with
permanent ileostomy =>The colon rectum and
anus are removed and followed by closure of
anus.
225
226. B) Regional Enteritis /crohn’s disease
• An inflammatory diseases of the small
intestine (60%) and colon or both.
• it involves all layers of the bowel but most
commonly involves the terminal ileum.
• It results in sever diarrhea and mal absorption
of vital nutrients.
226
227. c/ms
• In RE, the onset of
symptoms is usually
insidious
• abdominal pain and
diarrhea unrelieved by
defecation
• Crampy abdominal pain
• Abdominal tenderness
and spasm
• Since eating stimulates
peristalsis, the crampy
pain occur after meals
• Weight loss as a reason
of to avoids the crampy
pain, malnutrition and
secondary anemia.
227
229. Comparison b/n RE and UC
Ulcerative colitis
• Begins in the rectum
and proceeds in a
continuous manner
toward the colon
• Etiology: Un known
• 10-20 liquid bloody
stool per day
Regional enteritis
• Most often in the
terminal ileum with
patchy involvement
through all layers of the
bowel
• Un known
• 5-6 soft loose stools per
day rarely bloody
229
231. Cancer of large intestine colon and rectum
• The exact cause of colon and rectal cancer is
unknown.
but the risk factors including
• family history colon CA,
• history of chronic inflammatory diseases
• Age – over 40 ,
• Diet –high in fat, protein, beef, and low in
fiber .
231
232. Cont---
Distribution of cancer site throughout the
colon
• 22% in ascending colon,
• 11% transverse colon,
• 6% descending colon,
• 33% sigmoid colon and in 27% rectum
232
235. Clinical manifestations
• Changes in bowel habits
(most common)
• The passage of blood in
the stools (2nd most
common)
• Rectal/ abdominal pain,
• Tensmus and feeling of
incomplete emptying
after bowel mov’t.
Symptoms may include
also
• Unexplained anemia
• Wt loss , fatigue and
dull abdominal pain
235
236. Cont---
• N.B any patient with a history of unexplained
change in bowel habit, with passage of blood
in the stools should be studied carefully to
rule out cancer of the large bowel.
236
237. Diagnostic Evaluation
• Abdominal and rectal examination
• Fecal occult blood testing (most important)
• Procto sigmoidoscopy and colonoscopy with
biopsy or cytological smear)
• X-ray
237
238. Management
• Chemotherapy (anti carcinogenic drugs: IV-5
fluorouracil (5-FU), with or without Leucovorin ,
potent analgesics)
• Radiation therapy and supportive therapy
• Surgical resection of the affected area with
anastomosis /creation of a colostomy(fecal diversion)
if necessary : permanent or temporarily colostomy,
collectomy (colon removal )
238
239. Disease of the Anorectum
• Anorectal disorders are common.
It includes
• Anal Fissure
• anal fistula
• Anorectal Abscess and
• Hemorrhoids
239
240. Anal Fissure
• Is a longitudinal tear or ulceration in the lining
of the anal canal
• They are usually caused by the trauma of
passing a large, firm stool or from persistent
tightening of the anal canal because of stress
and anxiety
240
241. Cont---
Other causes includes
• Child birth
• Trauma and
• Over use of laxatives
c/ms
• Extreme painful defection, burning and
bleeding characterize fissures.
241
242. Cont---
• Most of these fissures heal if treated by
conservative measures, w/c include stool
softeners , an increase in water intake, sitz
bath and suppositories.
• If fissures do not respond to conservative Rx,
surgery is indicated.
• The anal sphincter is dilated and the fissure is
excised.
242
243. Anal fistula
• An anal fistula is a tiny, tubular, fibrous tract
that extends into the anal canal from anal an
opening located beside the anus.
• Fistulas usually result from an infection.
• They may also develop from trauma, fissures
or regional enteritis (RE) and obstructed
labuor in mother
243
244. C/ms
• Pus or stool may leak constantly from the
cutaneous opening.
• Other symptoms may be the passage of flatus
or feces from the vaginal or bladder
depending on the fistula tract.
• Untreated fistula may cause systemic infection
with related symptoms .
244
245. Mgt
• Surgery is always recommended.
• Fistulectomy /excision of the fistulous tract
• Keep the pt NPO and rehydrate with IV
245
246. Hemorrhoids
• Are dilated portions of veins in the anal canal.
• They are very common.
• By the age of 50, 50% of people have
hemorrhoids to some extent
246
247. Predisposing factors
• Increased intra abdominal pressure in the
hemorrhoid tissue
pregnancy,
constipation,
internal abdominal tumors = pressure in rectal
and anus veins = dilation occurs
247
248. Cont---
They are classified into two types:-
• Internal hemorrhoids:- if it occurs above the
internal sphincter
• External hemorrhoids: - those appearing
outside the external sphincter.
248
250. C/ms
• Hemorrhoids cause itching and pain and are
the most common cause of bright red
bleeding with defection
• Feeling of mass or pressure in the anal canal.
• Edema and inflammation
250
251. Cont---
• External hemorrhoids: are associated with
severe pain from the inflammation and edema
caused by thrombosis(i.e. clotting of blood
within the hemorrhage)
• Internal hemorrhoids: are not usually painful
until they bleed or prolapsed when they
became enlarged
251
252. Management
• It can be relieved by good personal hygiene,
and by avoiding excessive straining during
defecation
• A high residue diet and increased fluid intake.
• Laxatives , suppositories
• Warm compress, Sitz bath and bed rest
252
253. Cont---
Surgical Rx is applied according to the
progress.
• The rubber band legation procedure: the
hemorrhoid portion above the
mucocutaneous lines is grasped with an
instrument and a small rubber band is then
supplied over the hemorrhoids , the tissue
becomes necrotic after several days and
sloughs off.
253
257. Group Assignment and presentation on
Pancreatic, hepatic and billary disorders
Group 1 and 6: [Liver]
• Hepatitis
• Liver cirrhosis
Group 2 and 4 : [Liver and pancreas]
• Liver abscess and
• Pancreatitis
Group 3 and 5 : [Billary]
• Cholecystitis and
• Cholelithiasis
258. Outlines of the assignment
• Definition
• Epidemiology
• Pathopsiology (if any)
• Etiology/cause and or risk factors
• Clinical manifestations
• Diagnosis
• Management
• Nursing intervention
• Prevention and control measures
262. Jaundice
• When the bilirubin concentration in the
blood is abnormally elevated, all the
body tissues, including the sclerae and
the skin, become tinged yellow or
greenish-yellow, a condition called
jaundice.
• Jaundice becomes clinically evident when
the serum bilirubin level exceeds 2.5
mg/dL. 262
263. Cont’d…..
• Increased serum bilirubin levels and jaundice may
result from impairment of hepatic uptake,
conjugation ofbilirubin, or excretion of bilirubin into
the biliary system.
• There are several types of jaundice: hemolytic,
hepatocellular, and obstructive jaundice, and
jaundice due to hereditary hyperbilirubinemia.
• Hepatocellular and obstructive jaundice are the two
types commonly associated with liver disease.
263
264. Hemolytic Jaundice
• Hemolytic jaundice is the result of an increased
destruction of the red blood cells, the effect of
which is to flood the plasma with bilirubin so
rapidly that the liver, although functioning
normally, cannot excrete the bilirubin as quickly
as it is formed.
• This type of jaundice is encountered in patients
with hemolytic transfusion reactions and other
hemolytic disorders.
264
265. Hepatocellular Jaundice
• Hepatocellular jaundice is caused by the
inability of damaged liver cells to clear normal
amounts of bilirubin from the blood.
• The cellular damage may be caused by hepatitis
viruses, other viruses that affect the liver (eg,
yellow fever virus, Epstein-Barr virus),
medications or chemical toxins (eg, carbon
tetrachloride, chloroform, phosphorus,
arsenicals, certain medications), or alcohol.
265
266. Obstructive Jaundice
• Obstructive jaundice resulting from
extrahepatic obstruction may be caused by
occlusion of the bile duct from a gallstone, an
inflammatory process, a tumor, or pressure
from an enlarged organ (eg, liver, gallbladder).
Hereditary Hyperbilirubinemia
• Increased serum bilirubin levels
(hyperbilirubinemia), resulting from any of
several inherited disorders, can also produce
jaundice.
266
267. Portal Hypertension
• Portal hypertension is the increased pressure
throughout the portal venous system that results
from obstruction of blood flow through the damaged
liver.
• Commonly associated with hepatic cirrhosis, it can
also occur with non-cirrhotic liver disease.
• Although splenomegaly (enlarged spleen) with
possible hypersplenism is a common manifestation
of portal hypertension, the two major consequences
of portal hypertension are ascites and varices.
267
269. Clinical Manifestations
• Increased abdominal girth and rapid weight
gain are common presenting symptoms of
ascites.
• The patient may be short of breath and
uncomfortable from the enlarged abdomen,
and striae and distended veins may be visible
over the abdominal wall.
• Umbilical hernias also occur frequently in
those patients with cirrhosis.
• Fluid and electrolyte imbalances are common.
269
270. Management
• Dietary modification- The goal of treatment
for the patient with Ascites is a negative
sodium balance to reduce fluid retention.
Diuretics
• Use of diuretics along with sodium restriction is successful in 90% of
patients with ascites.
• Spironolactone (Aldactone), an aldosterone-blocking agent, is most often
the first-line therapy in patients with ascites from cirrhosis.
• When used with other diuretics, spironolactone helps prevent potassium
loss.
• Oral diuretics such as furosemide (Lasix) may be added but should be used
cautiously, because long-term use may induce severe sodium depletion
(hyponatremia).
270
271. Bed Rest
• In patients with ascites, an upright posture is
associated with activation of the renin–angiotensin–
aldosterone system and sympathetic nervous system
• This causes reduced renal glomerular filtration and
sodium excretion and a decreased response to loop
diuretics.
• Therefore, bed rest may be a useful therapy,
especially for patients whose condition is refractory
to diuretics.
• Paracentesis
271
272. Transjugular Intrahepatic Porto systemic Shunt
• TIPS-is a method of treating ascites in which a
cannula is threaded into the portal vein by the
transjugular route (Fig. 39-6).
• Toreduce portal hypertension, an expandable
stent is inserted to serve as an intrahepatic
shunt between the portal circulation and the
hepatic vein.
272
273. Hepatic Encephalopathy and Coma
• It is called portosystemic encephalopathy (PSE)
• Is a life-threatening complication of liver
disease that occurs with profound liver failure.
Patients with this condition have no overt signs
of the illness but do have abnormalities on
neuropsychologic testing
273
274. Clinical Manifestations
• The earliest symptoms of hepatic
encephalopathy include minor mental changes
and motor disturbances.
• The patient appears slightly confused and
unkempt and has alterations in mood and sleep
patterns.
274
275. Cont’d…….
• The patient tends to sleep during the day and
has restlessness and insomnia at night.
• As hepatic encephalopathy progresses, the
patient may become difficult to awaken and
completely disoriented with respect to time
and place.
• With further progression, the patient lapses
into frank coma and may have seizures.
• Asterixis (flapping tremor of the hands) may
be seen in stage II encephalopathy 275
276. HEPATIC CIRRHOSIS
• Cirrhosis is a chronic disease characterized by
replacement of normal liver tissue with
diffuse fibrosis that disrupts the structure and
function of the liver.
276
277. • There are three types of cirrhosis or scarring of the
liver:
Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas. This is
most frequently caused by chronic alcoholism and is
the most common type of cirrhosis.
Postnecrotic cirrhosis, in which there are broad bands of
scar tissue. This is a late result of a previous bout of
acute viral hepatitis.
Biliary cirrhosis, in which scarring occurs in the liver
around the bile ducts. This type of cirrhosis usually
results from chronic biliary obstruction and infection
(cholangitis); it is much less common than the other
two types.
277
278. • The portion of the liver chiefly involved in
cirrhosis consists of the portal and the
periportal spaces, where the bile canaliculi of
each lobule communicate to form the liver
bile ducts. These areas become the sites of
inflammation, and the bile ducts become
occluded with inspissated (thickened) bile and
pus.
278
279. • The liver attempts to form new bile channels;
hence, there is an overgrowth of tissue made
up largely of disconnected, newly formed bile
ducts and surrounded by scar tissue.
279
280. Clinical Manifestations
• Signs and symptoms of cirrhosis increase in
severity as the disease progresses.
• Their severity is used to categorize the
disorder as compensated or decompensated
cirrhosis
280
281. • Compensated cirrhosis, with its less severe,
often vague symptoms, may be discovered
secondarily at a routine physical examination
• The hallmarks of decompensated cirrhosis
result from failure of the liver to synthesize
proteins, clotting factors, and other
substances and manifestations of portal
hypertension
281
283. • Liver Enlargement
• Early in the course of cirrhosis, the liver tends to be large,
• and the cells are loaded with fat. The liver is firm and has a
• sharp edge that is noticeable on palpation. Abdominal pain
• may be present because of recent, rapid enlargement of the
• liver, which produces tension on the fibrous covering of the
• liver (Glisson’s capsule). Later in the disease, the liver
decreases
• in size as scar tissue contracts the liver tissue. The
• liver edge, if palpable, is nodular.
283
284. • Portal Obstruction and Ascites
• Portal obstruction and ascites, late
manifestations of cirrhosis,
• are caused partly by chronic failure of liver
function and
• partly by obstruction of the portal circulation.
284
285. • Infection and Peritonitis
• Bacterial peritonitis may develop in patients with cirrhosis
• and ascites in the absence of an intra-abdominal source of
• infection or an abscess. This condition is referred to as
• spontaneous bacterial peritonitis (SBP). Bacteremia due to
• translocation of intestinal flora is believed to be the most
• likely route of infection.
285
286. • Gastrointestinal Varices
• The obstruction to blood flow through the
liver caused by
• fibrotic changes also results in the formation
of collateral
• blood vessels in the GI system and shunting of
blood from
• the portal vessels into blood vessels with
lower pressures
286
287. • Edema
• Another late symptom of cirrhosis is edema,
which is attributed
• to chronic liver failure. A reduced plasma
albumin concentration
• predisposes the patient to the formation of
• edema.
287
288. • Vitamin Deficiency and Anemia
• Because of inadequate formation, use, and
storage of certain vitamins (notably vitamins
A, C, and K), signs of deficiency are common,
particularly hemorrhagic phenomena
associated with vitamin K deficiency.
288
289. • Mental Deterioration
• Additional clinical manifestations include
deterioration of
• mental and cognitive function with impending
hepatic encephalopathy
• and hepatic coma, as previously described
289
290. Management
• Antacids or histamine-2 (H2) antagonists are
prescribed to decrease gastric distress and
minimize the possibility of GI bleeding.
• Vitamins and nutritional supplements
promote healing of damaged liver cells and
improve the patient’s general nutritional
status.
• Potassium-sparing diuretics such as spironolactone or triamterene
(Dyrenium) may be indicated to decrease ascites, if present; these
diuretics are preferredbecause they minimize the fluid and electrolyte
changescommonly seen with other agents
290
291. Nursing Management
• Promoting Rest
• Reducing Risk of Injury
• Improving Nutritional Status
• Providing Skin Care
• Monitoring and Managing Potential Complications
Fluid Volume Excess
Hepatic Encephalopathy
Bleeding and Hemorrhage
• The patient is at increased risk for bleeding and hemorrhage because of
decreased production of prothrombin and decreased ability of the
diseased liver to synthesize the necessary substances for blood
coagulation.
291
292. DISORDERS OF THE GALLBLADDER
• Gallbladder disease with gallstones is the
most common disorder of the biliary system.
• Although not all occurrences of gallbladder
inflammation (cholecystitis) are related to
gallstones (cholelithiasis), more than 90% of
patients with acute cholecystitis have
gallstones.
292
294. Cholecystitis
• Cholecystitis, acute inflammation of the
gallbladder, causes pain, tenderness, and
rigidity of the upper right abdomen that may
radiate to the midsternal area or right
shoulder and is associated with nausea,
vomiting, and the usual signs of an acute
inflammation.
• An empyema of the gallbladder develops if
the gallbladder becomes filled with purulent
fluid (pus). 294
295. Cont….
• In calculous cholecystitis, a gallbladder stone
obstructs bile outflow.
• Bile remaining in the gallbladder initiates a chemical
reaction; autolysis and edema occur; and the blood
vessels in the gallbladder are compressed,
compromising its vascular supply.
• Gangrene of the gallbladder with perforation may
result.
• Bacteria play a minor role in acute cholecystitis;
however, secondary infection of bile occurs in
approximately 50% of cases. 295
296. • The organisms involved
• are generally enteric (normally live in the GI
tract) and include
• Escherichia coli, Klebsiella species, and
Streptococcus.
• Bacterial contamination is not believed to
stimulate the actual
• onset of acute cholecystitis (
296
298. Cholelithiasis
• Calculi, or gallstones, usually form in the
gallbladder from the solid constituents of bile;
they vary greatly in size, shape, and
composition (Fig. 40-2).
• They are uncommon in children and young
adults but become more prevalent with
increasing age, affecting 30% to 40% of people
by the age of 80 years.
298
299. Pathophysiology
• There are two major types of gallstones: those composed
• predominantly of pigment and those composed primarily of
• cholesterol. Pigment stones probably form when
unconjugated
• pigments in the bile precipitate to form stones; these
• stones account for about 10% to 25% of cases in the United
• States (Feldman, et al., 2006). The risk of developing such
• stones is increased in patients with cirrhosis, hemolysis, and
• infections of the biliary tract. Pigment stones cannot be
dissolved
• and must be removed surgically.
299
300. • Cholesterol stones account for most of the remaining
• 75% of cases of gallbladder disease in the United States.
• Cholesterol, a normal constituent of bile, is insoluble in water.
• Its solubility depends on bile acids and lecithin
(phospholipids)
• in bile. In gallstone-prone patients, there is decreased
• bile acid synthesis and increased cholesterol
• synthesis in the liver, resulting in bile supersaturated with
• cholesterol, which precipitates out of the bile to form
• stones.
300
301. • Two to three times more women than men develop
cholesterol
• stones and gallbladder disease; affected women are
• usually older than 40 years of age, multiparous, and
obese.
• Stone formation is more frequent in people who use
oral
• contraceptives, estrogens, or clofibrate; these
medications
• are known to increase biliary cholesterol saturation.
301
303. Clinical Manifestations
• Gallstones may be silent, producing no pain
and only mild
• GI symptoms. Such stones may be detected
incidentally
• during surgery or evaluation for unrelated
problems.
303
304. • The patient with gallbladder disease resulting from gallstones
• may develop two types of symptoms: those due to
• disease of the gallbladder itself and those due to obstruction
• of the bile passages by a gallstone. The symptoms may be
• acute or chronic. Epigastric distress, such as fullness,
abdominal
• distention, and vague pain in the right upper quadrant
• of the abdomen, may occur. This distress may follow a
• meal rich in fried or fatty foods.
304
305. • Pain and Biliary Colic
• Jaundice
• Changes in Urine and Stool Color
• Vitamin Deficiency
305
307. Medical Management
• The major objectives of medical therapy are to
reduce the
• incidence of acute episodes of gallbladder pain and
cholecystitis
• by supportive and dietary management and, if
possible,
• to remove the cause of cholecystitis by
pharmacologic
• therapy, endoscopic procedures, or surgical
intervention.
307
308. • Although nonsurgical approaches eliminate risks associated
• with surgery, these approaches are associated with persistent
• symptoms or recurrent stone formation. Most of the
nonsurgical
• approaches, including lithotripsy and dissolution of
• gallstones, provide only temporary solutions to gallstone
• problems and are infrequently used in the United States. In
• some instances, other treatment approaches may be
indicated;
• these are described later.
308
309. • Removal of the gallbladder (cholecystectomy) through
• traditional surgical approaches was the standard treatment
• for more than 100 years. It has largely been replaced by
laparoscopic
• cholecystectomy (removal of the gallbladder
• through a small incision through the umbilicus). As a result,
• surgical risks have decreased, along with the length of
• hospital stay and the long recovery period required after
• standard surgical cholecystectomy. In relatively rare instances,
• a standard surgical procedure may be necessary.
309
310. • Nutritional and Supportive Therapy
• Approximately 80% of the patients with acute gallbladder
• inflammation achieve remission with rest, IV fluids,
nasogastric
• suction, analgesia, and antibiotic agents. Unless the
• patient’s condition deteriorates, surgical intervention is
delayed
• just until the acute symptoms subside (usually within
• a few days). At this time, the patient should undergo a
laparoscopic
• cholecystectomy
310
311. • Pharmacologic Therapy
• Ursodeoxycholic acid (UDCA [URSO, Actigall])
and chenodeoxycholic
• acid (chenodiol or CDCA [Chenix]) have
• been used to dissolve small, radiolucent
gallstones composed
• primarily of cholesterol.
311
Fungus leave as a normal flora in immuno-competent pt with limited growth (there growth is limited by bacteria's in wait area and by natural dryness in skin, moist favor their growth)
Mucosal, skin, systemic , (systemic is fatal but rare)
40% of cases has family history of oral ulcer
No therapy is curative only alleviating the symptoms
Syrup is preferable (it will have a topical effect)
Pain 1st vomiting 2nd fever 3rd
1) Rebound tenderness: sever pain on quickly withdrawing of the palpating hand from the RLQ
2) Check for Rovsing’s sing: Pain in the right lower guardant during left- sided pressure suggests appendicitis (a positive Rovsing’s sign).
3) Look for psoas sign: Place your hand just above the patient’s right knee and ask the patient to raise the thigh against your hand.
Increased abdominal pain on this maneuver constitutes a positive psoas sign, suggesting irritation of the psoas muscle by an inflamed appendix.
4) Obturator sign: rotate leg internally and external with flexed hip and knee: right hypo gastricpain = positive obturator sign
The vasodilation that occurs in the splanchnic circulation
(the arterial supply and venous drainage of the GI
system from the distal esophagus to the midrectum including
the liver and spleen) is also a suspected causative factor. The
failure of the liver to metabolize aldosterone increases
sodium and water retention by the kidney. Sodium and water
retention, increased intravascular fluid volume, increased
lymphatic flow, and decreased synthesis of albumin by the
damaged liver all contribute to the movement of fluid from
the vascular system into the peritoneal space. The process
becomes self-perpetuating; loss of fluid into the peritoneal
space causes further sodium and water retention by the kidney
in an effort to maintain the vascular fluid volume.
As a result of liver damage, large amounts of albuminrich
fluid, 15 L or more, may accumulate in the peritoneal
cavity as ascites. (Ascites may also occur with disorders such
as cancer, kidney disease, and heart failure.) With the
movement of albumin from the serum to the peritoneal cavity,
the osmotic pressure of the serum decreases. This, combined
with increased portal pressure, results in movement of
fluid into the peritoneal cavity (Fig. 39-4).
