2. Enabling Objectives
At the end of this session you will be able to:
Discuss
Etiology,
Pathophysiology,
Clinical manifestations,
Complications,
Collaborative care, and
Nursing management of patients with Gastritis &
PUD, Acute Intestinal inflammatory Disorders,
Intestinal obstruction, selected hepatic disorders
2
By: Temamen T.
2/9/2024
4. Definition
PUD is an excavation (hollowed-out area)
that forms in the mucosal wall of the stomach,
in the pylorus, duodenum, or in the
esophagus
Results from the digestive action of HCl &
pepsin
More common in people b/n 40 & 60 years
Incidence
Is relatively uncommon in women of
childbearing age
Is almost equal to that in men after
menopause
Can occur without excessive acid secretion 4
By: Temamen T.
2/9/2024
6. Types of PUD
Depending on the degree of mucosal involvement
i. Acute PUD
Associated with superficial erosion and minimal
inflammation
ii. Chronic PUD
Is of long duration, eroding through the muscular
wall with the formation of fibrous tissue
Present continuously for many months or
intermittently throughout the person’s lifetime
Is at least four times as common as acute erosion
Depending on the location of erosion
a. Gastric ulcer (GU)
b. Duodenal ulcer (DU) 6
By: Temamen T.
2/9/2024
8. Cause
Infection with H. pylori
Excessive secretion of HCl in the stomach
because of:
Psychological stress (e.g., anxiety) and
physiological stress (like in case of burn,
shock, surgery)
Ingestion of milk and caffeinated
beverages
Ingestion of hot, rough, or spicy foods
Alcohol
8
By: Temamen T.
2/9/2024
9. Cause Cont’d…
Ulcerogenic drugs
Tumors, like in case of Zollinger-Ellison
syndrome (ZES)– produce excessive amounts
of the hormone gastrin
GERD- resulting in esophageal ulcer
Familial tendency-genetic link– those with
blood type O
Pregnancy appears to protect women from the
developing ulcers
9
By: Temamen T.
2/9/2024
11. Pathophysiology
Acids, bile salts, aspirin, ischemia, H. pylori
Breakdown of gastric mucosal barrier
Acid back-diffusion into mucosa
Destruction of mucosal cells
Acid & Pepsin release
Further mucosal erosion
Destruction of B/Vs
Bleeding
Histamine release
from damaged
mucosa
Vasodilation
Capillary
permeability
Loss of plasma
proteins into gastric
lumen
Mucosal edema
ULCERATION
11
By: Temamen T.
2/9/2024
12. Clinical Manifestations
Symptoms may last for a few days,
weeks, or months and may disappear only
to reappear, often without an identifiable
cause
12
By: Temamen T.
2/9/2024
13. C/Ms Cont’d…
Pain of duodenal
ulcer origin
Burning” or
“cramping”
Often located in the
mid-epigastrium
region beneath the
xyphoid process
Back pain
Usually relieved by
eating
Pain of gastric ulcer
origin
Located high in the epi-
gastrium
Occurs about 1 to 2
hours after meals
Can be burning” or
“gaseous”
Dull, gnawing pain or a burning sensation in
the mid-epigastrium or in the back
13
By: Temamen T.
2/9/2024
14. C/Ms Cont’d…
Sharply localized tenderness
Around the epigastrium or
Slightly to the right of the midline
Pyrosis (heartburn)
Emesis often containing undigested food
eaten many hours earlier
Bleeding– melana (tarry stools)
Abdominal distention
14
By: Temamen T.
2/9/2024
15. Emergency Complications
3 major emergency complications of PUD
1.Hemorrhage
2.Perforation(common in DU)
3.Gastric outlet obstruction
15
By: Temamen T.
2/9/2024
16. Complications Cont’d…
1. Hemorrhage
Is the first most common observed
Cause
Erosion of the granulation tissue
found at the base of the ulcer during
healing
Erosion of the ulcer through a major
blood vessels 16
By: Temamen T.
2/9/2024
17. Complications Cont’d…
2. Perforation
The 2nd most common complication
Commonly seen in large penetrating DUs
Occurs with ulcer penetrating the serosal
surface, with spillage of either gastric or
duodenal contents in to the peritoneal cavity
S/S
Sudden, severe upper abdominal pain that
quickly spread throughout the abdomen
Shallow and rapid respiration
Usually absent bowel sounds
Nausea and vomiting 17
By: Temamen T.
2/9/2024
18. Complications Cont’d…
3. Gastric outlet obstruction
Is the least common ulcer-related complication
Cause
Inflammation and edema in the peri-pyloric
region
S/s
Long history of ulcer pain
Pain
Short duration or completely absent
More generalized upper abdominal discomfort
that becomes worse towards the end of the
day as they fills and dilates
May be relieved by belching or by self-
18
By: Temamen T.
2/9/2024
19. Complications Cont’d…
S/s of Gastric outlet obstruction
Vomiting- which is very common and
often projectile
Constipation- as result of dehydration
Swelling in the upper abdomen as a
result of dilation of stomach
Loud peristalsis may be heard
19
By: Temamen T.
2/9/2024
20. Duodenal vs Gastric Ulcers
Duodenal Ulcer Gastric Ulcer
Lesion
Superficial; smooth margins;
round, oval, or cone shaped
Penetrating
Incidence
Age 30–60
Male: female 2–3:1
80% of peptic ulcers
Usually 50 and over
Male: female 1:1
15% of peptic ulcers
Risk Factors
H. pylori, alcohol, smoking,
stress
H. pylori, gastritis, alcohol,
smoking, use of NSAIDs, stress
20
By: Temamen T.
2/9/2024
21. GUs Vs DUs Cont’d…
Signs, Symptoms, and Clinical Findings
Hypersecretion of HCl
May have weight gain
Pain occurs 2-3 hrs after a meal
Often awakened b/n 1-2 AM
Ingestion of food relieves pain
Vomiting is uncommon
Hemorrhage less likely
Melena more common than
hematemesis
More likely to perforate
Normal—hyposecretion of HCl
Weight loss may occur
Pain 1⁄2 -1 hr after a meal
Rarely occurs at night
May be relieved by vomiting
Ingestion of food does not help
Vomiting common
Hemorrhage more likely
Hematemesis more common than
melena
Malignancy Possibility
Rare Occasionally
Duodenal Ulcer Gastric Ulcer
21
By: Temamen T.
2/9/2024
22. Diagnosis
Fiberoptic endoscopy
To visualize inflammatory changes, ulcers,
and lesions
To obtain a biopsy of the gastric mucosa
Upper GI barium-contrast study
Gastric secretory studies
CBC – determine anemia secondary to
bleeding
Liver enzyme studies
Stool tests – for the presence of blood
Serologic test for antibodies to the H. pylori 22
By: Temamen T.
2/9/2024
23. Management
Aim of the treatment
1.To decrease the amount of gastric
acidity
2.To enhance mucosal defense
mechanisms
3.To minimize the harmful effects on the
mucosa
23
By: Temamen T.
2/9/2024
26. Mgt Cont’d…
Nutritional Management
Avoiding irritant foods
and beverages
Hot, spicy foods and
pepper
Alcohol
Carbonated
beverages
Tea and coffee
Foods high in roughage,
such as raw fruits,
salads, and vegetables
Proteins
Best neutralizing
food
Stimulates HCl
secretion
Carbohydrates
and fats
The least to
stimulate HCl
secretion
Don’t neutralize
well
26
By: Temamen T.
2/9/2024
27. Nutritional Mgt Cont’d…
Milk
Milk proteins and calcium are stimulant to
gastric acid production
Can neutralize gastric acidity
Contains prostaglandins and growth factors
which protect the GI mucosa from injury
NB
i. No specific diet seems totally appropriate in
the treatment of ulcer disease
ii.Each patient should be instructed to eat and
drink foods and fluids that do not cause and
distressing or harmful side effects
27
By: Temamen T.
2/9/2024
28. Mgt Cont’d…
Pharmacologic Therapy
1. Neutralizing agents – Antiacids
Are the initial drugs of choice
Decrease gastric acidity and the acid content
of chyme reaching the duodenum
Block the conversion of pepesinogen to
pepsin by raising the pH to above 3.5
Some (like Al(OH)3) can bind to bile salts and
decrease their effects on the gastric mucosa
Examples: Aluminum hydroxide and
magnesium trisilcates 28
By: Temamen T.
2/9/2024
29. Pharmacologic Mgt Cont’d…
II. Antisecretory
a. Histamine H2-receptor antagonists
Inhibit the action of histamine at histamine H2
receptor cells to reduce the secretion of
gastric acid and total pepsin output
Ex: cimetidine, famotidine, nizatidine, ranitidine
b. Proton pump inhibitors (H+, K+-ATPase
inhibitors)
Inhibit the H+, K+-ATPase enzyme systemat
at the secretory surface of the gastric parietal
cells.
Block the last step of acid production
Ex: Omeprazole, Lansoprazole, Rabeprazole 29
By: Temamen T.
2/9/2024
30. Pharmacologic Mgt Cont’d…
III. Cytoprotective
Sucralfate
Accelerate healing
Doesn’t have acid neutralizing effect
Should be given at least 30 minutes
before or after an antiacid
Misoprostol
Is a synthetic prostaglandin
Protects the gastric mucosa
s mucus production and bicarbonate levels
Bismuth subsalicylate
Suppresses H. pylori bacteria 30
By: Temamen T.
2/9/2024
32. PUD Rx-- FMHACA-Ethiopia
I. PUD only
First Line
Omeprazole
20 mg P.O. QD for 4 weeks (DU) or 8 weeks (GU)
Alternatives
Cimetidine
400 mg P.O. BID, with breakfast and at night, OR
800 mg at night for 4 - 8 weeks
OR
Ranitidine
150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks
Maintenance therapy: 150 mg at bedtime.
OR
Famotidine, 40 mg, P.O. at night for 4-6 weeks
32
By: Temamen T.
2/9/2024
33. Pharmacologic Mgt Cont’d…
II. PUD associated with H. pylori
First Line
Amoxicillin, 1g, P.O. BID
PLUS
Clarithromycin, 500mg P.O. BID
PLUS
Omeprazole, 20mg P.O. BID (OR 40mg QD)
All for 7 - 14 days
Alternative
Clarithromycin, 500mg P.O. BID
PLUS
Metronidazole, 500mg, P.O. BID
PLUS
Omeprazole, 20mg P.O. BID OR 40mg QD for 7-14
days
33
By: Temamen T.
2/9/2024
34. Mgt Cont’d…
Surgical Management
Usually recommended for:
Patients with intractable ulcers
Those that fail to heal after 12 to 16 weeks of
medical treatment
Life-threatening hemorrhage, perforation, or
obstruction
Those with ZES not responding to medications
Types
1. Pyloroplasty- the pylorus, is cut and resutured, to
relax the muscle and widen the opening into the
intestine.
2. Vagotomy
3. Antrectomy
Gastroduodenostomy
Gastrojejunostomy 34
By: Temamen T.
2/9/2024
36. Nursing Management
1. Acute pain related to the effect of gastric
acid secretion on damaged tissue
2. Imbalanced nutrition, less than body
requirement related to changes in diet
3. Deficient knowledge about prevention of
symptoms and management of the
condition 36
By: Temamen T.
2/9/2024
37. Nursing Interventions
1. Relieving Pain
Patient education:
To take the prescribed drugs
To avoid aspirin, foods and beverages that
contain caffeine
To eat meals at regularly paced intervals in
a relaxed setting
Teaching relaxation techniques to help
manage stress and pain
Enhance smoking cessation efforts
37
By: Temamen T.
2/9/2024
38. Nsg Interventions Cont’d…
2. Maintaining Optimal Nutritional
Status
Assesses the patient for malnutrition and
weight loss
Advise the patient about the importance
of complying with the medication regimen
and dietary restrictions
38
By: Temamen T.
2/9/2024
39. Nsg Interventions Cont’d…
3. Teaching Patients Self-Care
Factors that will help or aggravate the
condition
Drug information
Avoiding foods that exacerbate symptoms
and potentially acid-producing foods
Eating meals at regular times and in a relaxed
setting
Avoiding overeating
Irritant effects of smoking on the ulcer and
cessation of smoking 39
By: Temamen T.
2/9/2024
40. Nsg Interventions Cont’d…
Teach about the S/S of complications:
i. Hemorrhage
cool skin, confusion, ed heart rate, ed
BP, labored breathing, blood in stool
ii. Penetration and perforation
Severe abdominal pain, rigid and tender
abdomen, vomiting, ed temp, ed HR
iii. Pyloric obstruction
Nausea and vomiting, distended abdomen,
abdominal pain
40
By: Temamen T.
2/9/2024
43. Introduction
The Appendix
A small, finger-like appendage about 7 cm (3
inch) long
Attached to the cecum just below the ileo-
cecal valve
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
43
By: Temamen T.
2/9/2024
44. Definition
Appendicitis- is an inflammation of the
vermiform appendix
Etiology
Obstruction of the lumen by:
A fecalith (accumulated feces)-common
Foreign bodies
Worms (e.g., Pinworms, ascaris)
Intramural thickening caused by lymphoid
hyperplasia
Tumors of the cecum or appendix
44
By: Temamen T.
2/9/2024
46. Clinical Manifestations
Vague epigastric or peri-umbilical pain
Progressing to RLQ
May be accompanied by:
A low-grade fever
Nausea and vomiting
Loss of appetite
Local tenderness is elicited at McBurney’s
point when pressure is applied
Guarding the abdominal area by lying still with
the right leg flexed at the knee
46
By: Temamen T.
2/9/2024
49. Possible signs of Appendicitis
a. Rebound tenderness
b. Rovsing’s sign &
referred rebound
tenderness
Press deeply and evenly
in the LLQ
Then quickly withdraw
your fingers
49
Rebound
tenderness:
Suggests
peritoneal
inflammation, as
from appendicitis
Pain in the RLQ during left-sided pressure
Positive Rovsing’s sign
RLQ pain on quick withdrawal
Referred rebound tenderness
2/9/2024
50. c. Positive Psoas Sign
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 stretches50
By: Temamen T.
2/9/2024
52. Possible Appendicitis…
d. 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
52
By: Temamen T.
2/9/2024
54. Possible Appendicitis…
If the appendix has ruptured
The pain becomes more diffuse
Abdominal distention develops
The patient’s condition worsens
2/9/2024 By: Temamen T. 54
55. C/Ms Cont’d…
The extent of tenderness depends on the
location of the inflamed appendix
Pain on defecation suggests that the tip of
the appendix is resting against the rectum.
Pain in urination suggest that the tip is near
to the bladder
If tip is in the pelvis can be elicited only on
rectal examination.
55
By: Temamen T.
2/9/2024
56. Acute Complications
a. Perforation
The most common and generally
occurs 24 hours after the onset of
pain
b. Peritonitis
c. Abscess
56
By: Temamen T.
2/9/2024
58. Management
Surgery is indicated if appendicitis is
diagnosed
Antibiotics and intravenous fluids
To correct or prevent fluid and electrolyte
imbalance and dehydration, until surgery is
performed
Used for 6 to 8 hrs before the
appendectomy If the appendix has
ruptured and there is evidence of
peritonitis or an abscess
Analgesics after diagnosis
Appendectomy 58
By: Temamen T.
2/9/2024
60. Nursing Management
Patient preparation for surgery
IV infusion to replace fluid loss and promote
adequate renal function
Antibiotic therapy to prevent infection
Enema is not administered because risk of
perforation
Avoid self-treatment like the use of laxatives
and enema to prevent perforation
Cold compress to the RLQ to decrease blood flow
to the area and impend the inflammatory process
Heat is never used because it may cause the
appendix to rupture
60
By: Temamen T.
2/9/2024
61. Nsg Mgt Cont’d…
Postoperative care
Placing the patient in a semi-Fowler
position
Opioid, usually morphine sulfate
Oral fluids as tolerated
Food is provided as desired and tolerated
on the day of surgery
Ambulation begins the day of surgery or the
first postoperative day
Discharge on the first or second
postoperative day
Normal activities are resumed 2 to 3 weeks
after surgery 61
By: Temamen T.
2/9/2024
62. Peritonitis
Is an inflammation of the peritoneum
Causes
The most common causative organisms:
Escherichia coli
Klebsiella
Proteus
Pseudomonas
Others organisims:
Streptococci spp
Staphylococci
Pneumococci
62
By: Temamen T.
2/9/2024
63. Cause Peritonitis Cont’d…
It can result from
Diseases of the GI tract
From the internal reproductive organs (females)
External sources
Injury or trauma (e.g., gunshot wound, stab
wound)
Extension from the inflammation of retroperitoneal
organs like the kidneys
Appendicitis
Perforated ulcer
Diverticulitis
Bowel perforation
63
By: Temamen T. 2/9/2024
64. Clinical Manifestations
Symptoms depend on the location and
extent of the inflammation
S/S include:
Pain
At first diffuse type
Tends to become constant, localized,
and more intense near the site of the
inflammation.
Usually aggravated by movement
64
By: Temamen T.
2/9/2024
65. C/Ms Cont’d…
The affected area of the abdomen becomes
extremely tender and distended, and the
muscles become rigid
Rebound tenderness
Nausea and vomiting
Peristalsis is diminished
Increased temperature and pulse rate
Almost always an elevated leukocyte count
65
By: Temamen T.
2/9/2024
66. Diagnosis
Lab tests
Increased leukocyte count
ed Hemoglobin and hematocrit
blood loss
Serum electrolyte studies
Abdominal x-ray
CT scan of the abdomen
Peritoneal aspiration and culture
66
By: Temamen T.
2/9/2024
67. Complications
1.Sepsis-- the major cause of death
2.Shock- due to septicemia or hypovolemia
3.Intestinal obstruction with bowel adhesion as
a result of the inflammatory process
4.Wound evisceration/dehiscence and abscess
formation
S/S
Tender or painful abdomen
Feeling as if something just gave way
67
By: Temamen T.
2/9/2024
68. Management
Administration of several liters of an
isotonic solution
Analgesics
Anti-emetics
Intestinal intubation and suction
Oxygen therapy by nasal cannula or
mask
68
By: Temamen T.
2/9/2024
69. Mgt Cont’d…
Large doses of IV broad-spectrum antibiotic
until the specific organism causing the
infection is identified
Third-generation cephalosporins
Cefotaxime
Ceftriaxone
Patients with primary bacterial peritonitis
(PBP) usually respond within 72 hours to
appropriate antibiotic therapy
Administered for as little as 5 days and can
be extended to 2 weeks course 69
By: Temamen T.
2/9/2024
70. Mgt Cont’d…
Surgery
To remove the infected material and correct
the cause
Includes:
Excision (i.e., appendix)
Resection with or without anastomosis (i.e.,
intestine)
Repair (i.e., perforation)
Drainage (i.e., abscess)
70
By: Temamen T.
2/9/2024
72. Intestinal Obstruction
A partial or complete blockage of the
bowel that prevents the normal flow of
intestinal contents through the intestinal
tract.
Two types:
Mechanical obstruction
Functional obstruction
72
By: Temamen T.
2/9/2024
73. Types of Intestinal Obstruction Cont’d…
A. Mechanical Obstruction(accounts for 90%)
Cause:
Intra-luminal obstruction or
Obstruction from pressure on the intestinal
walls
Examples:
1. Adhesions (50%)
Loops of intestine become adherent to areas
that heal slowly or scar after abdominal
surgery
May produce a kinking of an intestinal loop
73
By: Temamen T.
2/9/2024
74. Types of Intestinal Obstruction Cont’d…
2. Hernias (15%)
Protrusion of intestine through a weakened
area in the abdominal muscle or wall
May result in complete obstruction of
intestinal lumen and obstruction of blood flow
to the area
3. Intussusception(common in small bowel
obstruction)
One part of the intestine slips into another
part located below it
Results in narrowing of intestinal lumen
74
By: Temamen T.
2/9/2024
76. Types of Intestinal Obstruction Cont’d…
4. Volvulus(common in large bowel of
sigmoid colon)
Bowel twists and turns on itself
Results in obstruction to intestinal lumen
and accumulation of gas and fluid in the
trapped bowel
5. Others include:
Neoplasms (15%)
Stenosis
Strictures
Abscesses
76
By: Temamen T.
2/9/2024
77. Volvulus of the sigmoid colon
Types of Intestinal Obstruction Cont’d…
77
By: Temamen T.
2/9/2024
78. Types of Intestinal Obstruction
Cont’d…
B. Functional Obstruction
Intestinal musculature cannot propel the
contents along the bowel as result of
neuromuscular or vascular disorders
Examples:
Paralytic ilues (the most common)
Amyloidosis
Muscular dystrophy
Endocrine disorders such as diabetes
mellitus
Neurologic disorders such as Parkinson's 78
By: Temamen T.
2/9/2024
79. Small Intestine Obstruction
Accumulate of fluid, gas & intestinal contents proximal to the
obstruction
Abdominal distention and retention of fluid
Reduced absorption of fluids and stimulation of more gastric
secretions
Increased fluid in the lumen
Increased intraluminal pressure
Increase venous and arteriolar capillary pressure
Increased capillary permeability
Circulating blood
Hypovolemic
Shock
Edema, congestion,
necrosis
Perforation of the intestinal
wall
Peritonitis
Fluid and electrolyte extravasation to the peritoneal
cavity
79
By: Temamen T.
2/9/2024
80. Clinical Manifestations
Crampy pain that is wavelike and colicky
Severe, steady pain strangulation
In the absence of strangulation, the abdomen
is not tender
Passing blood & mucus, with no fecal matter &
no flatus
Unmistakable signs of dehydration
Abdominal distension
Nausea and vomiting
80
By: Temamen T.
2/9/2024
81. C/Ms Cont’d…
Vomiting
Bilious rapid projectile vomiting
obstruction located high in the small bowel
Vomiting of fecal material
Obstruction below the proximal colon or in
the ileum
Progression of the vomiting
Vomiting the Stomach contents
Then the bile-stained contents of the
duodenum & the jejunum
Finally, with each paroxysm of pain, the
darker, fecal-like contents of the ileum
81
By: Temamen T.
2/9/2024
82. Diagnosis
History and physical examination
Abdominal x-ray studies
CT-scan
Ultrasound
Biopsy
Laboratory studies
CBC
ed WBCs
Strangulation or perforation
ed hemoglobin or hematocrit
Bleeding from neoplasm or
strangulation with necrosis
Serum electrolyte profile 82
By: Temamen T.
2/9/2024
83. Medical Management
Decompression of the bowel through a naso-
gastric or small bowel
Surgical intervention
IV therapy before surgery to replace the
depleted water, sodium, chloride, and
potassium
Include:
Repairing the hernia
Dividing the adhesion
Removing the portion of affected bowel 83
By: Temamen T.
2/9/2024
84. Large Bowel Obstruction
Attributes to15% of intestinal
obstructions
Commonly occur in the sigmoid colon
The most common causes:
Carcinoma
Diverticulitis
Benign tumors
84
By: Temamen T.
2/9/2024
85. Clinical Manifestations
Unlike small intestine symptoms develop and
progress relatively slowly
Obstruction in the sigmoid colon or the rectum
Constipation in patients
Distention of the abdomen
Visible outlining of loops of large bowel
through the abdominal wall
Crampy lower abdominal pain
Fecal vomiting
Symptoms of shock may occur
85
By: Temamen T.
2/9/2024
86. Diagnosis
See under small bowel obstruction
Barium enema
To locate large intestinal obstruction
Not used if perforation is suspected
86
By: Temamen T.
2/9/2024
87. Management
Colonoscopy
Inspection of the interior surface of the
colon
To untwist and decompress the bowel.
Temporary or permanent colostomy
Ileoanal anastomosis
To remove the entire large colon
Rectal tube
To decompress an area that is lower in the
bowel 87
By: Temamen T.
2/9/2024
89. Hepatic Dysfunction
Hepatic dysfunction results from damage to
the liver’s parenchymal cells by:
Directly from primary liver diseases
Indirectly from obstruction of bile flow or
derangements of hepatic circulation
89
By: Temamen T.
2/9/2024
90. The most common and significant
symptoms of liver disease
1. Jaundice
2. Portal hypertension, ascites, and
varices
3. Nutritional deficiencies
4. Hepatic encephalopathy or coma
90
By: Temamen T.
2/9/2024
91. Jaundice/Icterus
Is yellowish-tinged or greenish-yellow
discoloration of the body tissues, including the
sclera, mucosa and the skin as result of
abnormal elevation of bilirubin concentration in
the blood.
Is a symptom rather than a disease
Becomes clinically evident when the serum
bilirubin level exceeds 2.5 mg/dL
May result from impairment of:
Hepatic uptake
Conjugation of bilirubin
91
By: Temamen T.
2/9/2024
92. Types of Jaundice
1. Hemolytic
2. Hepatocellular
3. Obstructive
4. Hereditary hyperbilirubinemia
92
By: Temamen T.
2/9/2024
94. I. Hemolytic/ Pre-hepatic Jaundice
Results from an increased destruction of
the RBC
Flood the plasma with unconjugated
bilirubin so rapidly
Causes
Hemolytic transfusion reactions
Sickle cell crisis
Hemolytic anemia
94
By: Temamen T.
2/9/2024
95. Hemolytic Jaundice Cont’d…
If prolonged it may result in:
The formation of pigment stones in
the gallbladder
Extremely severe jaundice (>20 to 25
mg/dl) poses a risk for brain stem
damage
Lab Tests
ed fecal and urine urobilinogen
Urine is free of bilirubin
95
By: Temamen T. 2/9/2024
96. II. Hepatocellular/ hepatic Jaundice
Caused by the inability of damaged liver
cells to:
Take up bilirubin from the blood or
Conjugate or
Excrete normal amount of bilirubin
from the blood
Eg, Cirrhosis
Patients may be mildly or severely ill
96
By: Temamen T.
2/9/2024
97. Hepatocellular Jaundice Cont’d…
Causes of cellular damage
Infection by viral hepatitis or other viruses
Medication or chemical toxicity or alcohol
Hepatic carcinoma
Lab Tests:
ed unconjugated serum bilirubin
ed AST & ed ALT levels
97
By: Temamen T.
2/9/2024
98. III. Obstructive / Post-hepatic Jaundice
Is due to obstructed flow of bile
A. Intra-hepatic obstruction
May involve obstruction of the small bile ducts
within the liver
Can be caused by
Pressure on these channels from inflammatory
swelling of the liver (hepatitis, cirrhosis,
tumors)
Inflammatory exudates within the ducts
themselves
98
By: Temamen T.
2/9/2024
99. Obstructive Jaundice Cont’d…
B. Extra-hepatic obstruction
Caused by occlusion of the bile duct by a
gallstone, an inflammatory process, a tumor,
or pressure from an enlarged organ
99
By: Temamen T.
2/9/2024
100. Obstructive Jaundice Cont’d…
Clinical Findings
Bile backed up into the liver substance
Reabsorbed into the blood
Carried throughout the entire body
Staining the skin, mucous membranes, and
sclera
Deep orange and foamy urine(increased urine
bilirubin
Light or clay-colored stool(decreased fecal
urobilirubin)
The skin may itch intensely 100
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2/
9/
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24
101. Obstructive Jaundice Cont’d…
Lab tests:
AST, ALT levels rise moderately
ed conjugated and unconjugated
bilirubin
ed urine bilirubin
ed to no fecal or urinary urobilinogen
101
By: Temamen T.
2/9/2024
104. Portal hypertension (PHpn)
Normal pressure in the portal vein is 5 to
10 mmHg
PHpn is commonly associated with
hepatic cirrhosis
It can also occur with noncirrhotic liver
disease like thrombosis, or clotting in the
portal vein
104
By: Temamen T.
2/9/2024
105. 105
Alcohol Abuse, Infection, Drugs, Bilary Obstruction
Destruction of Hepatocytes
Replacement of destroyed liver cells gradually by scar tissue
The amount of scar tissue exceeds that of the functioning liver tissue
Fibrosis/Scar
Impaired blood and lymph flow
ed pressure in the venous & sinusoidal channels
Fatty infiltration—fibrosis/scar
Portal Hypertension
PP
Splenomegaly
Jaundice
Ascites
BP
Esophageal varices
DHN
By: Temamen T.
2/9/2024
107. Ascites
Ascites is the accumulation of fluid in
the peritoneal cavity
Risk factors
Cirrhosis—for 80% of cases
Renal factors: stimulation of RAA
system
Other conditions like
Congestive heart failure
Nephrosis
107
By: Temamen T.
2/9/2024
108. PP
108
Portal Hypertension/Resistance
to Blood Flow
Leakage of plasma into
liver lymphatics
Vasocongestion within
intestinal vasculature
Development of collateral
venous vessels
Production of liver
lymph with high protein
Transudation of plasma
into the abdominal cavity
Persistence of amine
neurotransmitters
Leakage of lymph
into abdominal
cavity with osmotic
gradient between
lymph & ECF
Ascites
Redistribution of blood flow—
reduced renal perfusion
Stimulation of
RAA system
Sodium and water
retention
Leakage of plasma
out of vascular space
Intravascular oncotic pressure
Albumin production
Hepatocyte Dysfunction
Esophageal Varices
Hemorrhoids
109. Clinical Manifestations
ed abdominal girth
Bulging of flanks
Shifting dullness
Fluid wave/trill
Everted umbilicus (severe)
Rapid weight gain
SOB
Visible striae and distended veins over the
abdominal wall
Signs of dehydration
Decreased urine output 109
By: Temamen T.
2/9/2024
112. Diagnosis
History
Physical Examination
Diagnostic paracentesis (50 to 100 mL)
The fluid should be examined for its gross
appearance; protein content, cell count, and
differential cell count should be determined
Cytologic analysis
112
By: Temamen T.
2/9/2024
113. Management of Ascites
Dietary Modification
Diuretics- spironolactone, Lasix
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt
113
By: Temamen T.
2/9/2024
114. Esophageal Varices
A complex of longitudinal tortuous and
extremely dilated sub-mucosal veins at
the lower end of the esophagus,
enlarged and swollen as the result of
portal hypertension
The vessels are especially susceptible to
hemorrhage.
Bleeding or hemorrhage from
esophageal varices occurs in
approximately one third of patients with 114
115. Factors that contribute to hemorrhage
Muscular exertion from lifting heavy objects
Straining at stool
Sneezing, coughing, or vomiting
Esophagitis
Irritation of vessels by poorly chewed foods or
course foods or irritating fluids
Reflux of stomach contents (especially alcohol)
Salicylates and any medication that erodes the
esophageal mucosa
Liver cirrhosis
115
116. PP Esophageal Varices
Portal hypertension (caused by resistance to portal
flow and increased portal venous inflow)
Development of pressure gradient of >=12 mm Hg
between portal vein and inferior vena cava
(portal pressure gradient)
Venous collaterals develop from high portal system
pressure to systemic veins in esophageal plexus,
hemorrhoidal plexus and retroperitoneal veins
Abnormal varicoid vessels form in any of above
locations
Vessels may rupture causing life-threatening 116
118. Management
Intravenous fluids with electrolytes and
volume expanders
Oxygen is administered to prevent
hypoxemia/hypoxia
Monitoring vital signs continuously
Pharmacologic Therapy
Vasopressin (IV or intra-arterial)
Propranolol and nadolol, beta-blocking
agents that decrease portal pressure
Nitrates such as isosorbide
118
119. Hepatic Cirrhosis
Characterized by irreversible chronic
injury of the hepatic parenchyma
Extensive degeneration and destruction of the
liver parenchyma cells and by replacement of
liver tissue by fibrous scar tissue.
119
120. Types of cirrhosis or scarring of
the liver:
A. Alcoholic cirrhosis
Frequently due to chronic alcoholism for
decades, resulting in:
Chronic inflammatory
Toxic effects on the liver
Blocking the normal metabolism of
protein, fats, and carbohydrates
Scar tissue characteristically surrounds the
portal areas
Is the most common type of cirrhosis 120
121. Types of Cirrhosis Cont’d…
B. Postnecrotic cirrhosis
There are broad bands of scar tissue
as a late result of a previous bout of
acute viral hepatitis (hepatitis B or
hepatitis C)
C. Biliary cirrhosis
Scarring occurs in the liver around
the bile ducts
Is the result of chronic biliary
obstruction and infection 121
122. Clinical manifestation
Early manifestation
Palpation of liver reveals a firm, lumpy,
(nodular), usually enlarged liver.
GI disturbance – anorexia, nausea,
vomiting……
Hepatomegally
Pain
Late manifestation
Ascites, gastro intestinal bleeding from varices
Encephalopathy, splenomegally, jaundice, skin
lesion, Anemia
Sodium and fluid retention 122
124. Dx
Increased Serum bilirubin
Increased Serum ammonia: because of
inability to convert ammonia to urea.
Decreased Serum glucose: impaired
glycogenesis
Decreased Serum albumin
CBC: Hb/Hct and RBCs may be decreased
because of bleeding
Increased BUN: indicates breakdown of
blood/protein
124
125. Medical Management
Symptomatic management
Antacids—to decrease gastric distress and
minimize the possibility of GI bleeding.
Vitamins and nutritional supplements
Potassium-sparing diuretics (spironolactone,
triamterene)--to decrease ascites
Avoidance of alcohol
125
126. Hepatic Encephalopathy and Coma
Hepatic encephalopathy
Is a life-threatening complication of liver
disease occurring with profound liver failure
May result from the accumulation of ammonia
and other toxic metabolites in the blood
Can occur in any condition in which liver
damage causes ammonia to enter the
systemic circulation without liver detoxification
Hepatic coma represents the most advanced
stage of hepatic encephalopathy
126
By: Temamen T.
2/9/2024
127. Hepatic Encephalopathy cont’d…
Normally, the liver converts ammonia in to glutamine,
which is stored in the liver and later converted to urea
and excreted via the kidneys.
Blood ammonia rises when the liver cells are unable to
perform this conversion due to liver cell damage and
necrosis.
C/m
From mild mental confusion like, unresponsiveness,
forgetfulness, trouble concentrating, or changes in
sleep habits to deep coma.
Simple tasks, such as handwriting, become
difficult 127
By: Temamen T.
2/9/2024
128. Hepatic Encephalopathy cont’d…
Asterixis or “liver flap”. The patient is asked to
hold the arm out with the hand held upward
(dorsiflexed). Within a few seconds, the hand
falls forward involuntarily and then quickly
returns to the dorsiflexed position.
Dx
Lab-results show elevated blood
ammonia
128
By: Temamen T.
2/9/2024
129. Hepatic Encephalopathy cont’d…
Medical Management
Principles of intervention in hepatic
encephalopathy.
Reduce protein in the intestine
Prevent gastro-intestinal bleeding.
Reduce bacterial production of NH3 by neomycin
High cleansing enema to decrease bacteria.
Eliminate infection.
Intravenous administration of glucose to minimize
protein breakdown 129
By: Temamen T.
2/9/2024
Colostomy: a surgical procedure where a portion of the large intestine is brought through the abdominal wall to carry stool out of the body
Colonoscopy: inspection of the interior surface of the colon with a flexible endoscope that is equipped to obtain tissue samples and inserted through the rectum
Colectomy: surgical removal of the large bowel
