Dental plaque and caries are caused by bacteria in the mouth that metabolize sugars to produce acids. These acids demineralize tooth enamel over time, leading to cavities and damage. Proper oral hygiene through brushing, flossing, and professional cleanings can help remove plaque and prevent caries. Dietary choices like limiting sugar intake and drinking fluoridated water also reduce risk. Left untreated, caries can progress to pulpitis, abscesses, or tooth loss. Gingivitis is a mild form of gum inflammation due to plaque that can be reversed, while periodontitis involves deeper infection and bone loss requiring treatment to stop progression.

1. Management of
Patients with Oral
disorders
1

2. Dental Plaque and Caries
2
 Dental caries is a dietary carbohydrate-modified bacterial
infectious disease with saliva as a critical regulator.
 A process of demineralization of tooth enamel, leading
to destruction of enamel and dentin, with cavitations
of the tooth
Tooth decay
 Is localized progressive disease, whose character consists in the
destruction of tooth structures mainly under the influence of metabolic
products of the oral microflora;
 Is an erosive process begins with the action of bacteria on
fermentable carbohydrates in the mouth.
 Produces acids and dissolve tooth enamel

3. Dental caries----
3
 Dental caries and periodontal diseases result from the accumulation of
many different species of bacteria that form dental plaque
 Bacterial adhesion to surfaces primarily involves two types of
reactions: physicochemical and biochemical
The microorganisms within bacterial plaque can produce :
 Extracellular coatings, such as slime layers which prolong the
existence of biofilms ;
 A variety of surface fibrils, or appendages, that extend from their cell
walls.
 These mechanisms mediate attachment of bacteria to a substrate by
providing additional attachment structures between the tooth surface
and the plaque, thus allowing the formation of adherent matrices

4. Bacterial Colonization of the Mouth
4
 Microorganisms found in the oral cavity are naturally acquired from
the environment.
 Bacteria are acquired from the atmosphere, food, human contact.
 Bacteria form colonies between saliva and hard tissues such as
erupted teeth, and exposed root cementum and dentin.

5. The extent of damage to the teeth
depends on the following:
5
The presence of dental plaque
The strength of the acids and the ability of the saliva to
neutralize them
The length of time the acids are in contact with the teeth
The susceptibility of the teeth to decay

6. Dental plaque
6
Is the soft tenacious material found on tooth surfaces
which is not readily removed by rinsing with water”
Gluey, gelatin-like substance consisting of:
 Bacteria (lactobacilli and streptococcus mutans)
 Saliva, and
 Epithelial cells that adheres to the teeth.

7. Types of dental plaque by placement:
7
1. Dentogingival plaque (on the smooth
surfaces along the gingival margins)
2. Approximal dental plaque
3. Subgingival plaque
4. Occlusal or fissure plaque

8. PP-- Dental caries
8
Dental decay begins with small hole/fissure on teeth

Bacteria produce acids from the breakdown of sugars contained in food within
30 minutes after eating

Dental caries penetrate the enamel and extend to the underlying dentin

Cavitation of the enamel

Penetrate to the tooth pulp

Acute pulpitis

Infection of blood vessels, lymph vessels, and nerves

Abscess

Soreness, facial swelling and pulsating pain

9. Dental Plaque and Caries
9

10. Dental Plaque and Caries
10

11. Dental Plaque and
Caries
11

12. Treatment
12
Common treatments
Removal of the softened and infected hard tissues
Fillings
Dental implants
Extractions
Root canal therapy
 The contents of the pulp chamber and root canals are removed, followed by
thorough cleaning, antisepsis, and filling with an inert material

13. Prevention of Dental Carries
13
A. Mouth Care
 Normal mastication (chewing)
 Normal flow of saliva
 Brushing and flossing every day
 Wiping the teeth with a gauze pad
 Swishing the mouth with an antiseptic mouthwash several times before
expectorating

14. Prevention of Dental Carries Cont’d…
14
B. Diet
 Decreasing the amount of sugar and starch in the diet
 Snacks --less cariogenic alternatives
 Fruits
 Vegetables
 Cheeses

15. Prevention of Dental Carries Cont’d…
15
C. Fluoridation
 Public water supplies
 Applying a concentrated gel or solution to the teeth
 Adding fluoride to home water supplies
 Using fluoridated toothpaste or mouth rinse
 Using sodium fluoride tablets, drops, or lozenges
D. Pit and Fissure Sealants
 Applying a special coating to fill and seal pits and
fissures which last up to 7 years
E. Controlling diabetes

16. Gingivitis
16
 Lat. gingiva = gingie(gum); -itis = inflammation
 Gingivitis refers to gingival inflammation induced by bacterial
biofilms, also called plaque, adherent to tooth surfaces.
 Bacterial plaque accumulates in the spaces between the gums
and teeth and in calculus (tartar) that forms on the teeth.
 These accumulations may be tiny, even microscopic, but the
bacteria contained in them, produces foreign chemicals and
toxins that cause inflammation of the gums around teeth.
 Inflammation of the gum tissue- term used to describe non-
destructive periodontal disease

17. 17
A(Normal gum)
B(Gums are red and
swollen)

18. CLASSIFICATION OF GINGIVITIS
18
 Acute gingivitis
 Recurrent gingivitis
 Chronic gingivitis
Acute gingivitis:
 It is of sudden onset and short duration and can be painful
 A less severe form of acute condition is called sub-acute.
Recurrent gingivitis
 Reappears after eliminated by a treatment or disappearing
spontaneously.
Chronic gingivitis:
 Slow in onset and long duration
 Is painless
 Inflammation persists or resolves and normal areas become
inflamed

19. Cause
19
Poor oral hygiene resulting in food debris, bacterial plaque
accumulate
Missing or irregular teeth
Faulty dentistry
Smoking tobacco
Breathing through the mouth
Local trauma (e.g., an overly aggressive tooth brushing technique)
Dry mouth: because of loss of protective effect of saliva
Vitamin deficiency, especially of vitamin C

20. STAGES OF GINGIVITIS
20
STAGE I : THE INITIAL LESION(2-4 days)
 Vascular changes dilated capillaries and increased
blood flow.
 Initial inflammatory changes due to microbial activation
of resident leukocytes and stimulation of endothelial
cells.
STAGE II : THE EARLY LESION
 Clinical signs : ERYTHEMA[proliferation of capillaries and increased
formation of capillary loops between rete pegs].
• Evidence of bleeding on probing.
• Increase in gingival fluid flow and number of trans migrating
leukocytes[also T lymphocytes].
• Amount of collagen destruction increases which is related to Matrix
Metalloproteins


21. 21
STAGE III : THE ESTABLISHED LESION
Predominance of plasma cells and B lymphocyte.
Localised gingival anoxmia[impaired venous return](bluish
hue on the reddened gingiva).
Lesion is moderately to severely inflamed
STAGE IV : THE ADVANCED LESION
Extension of the lesion into the alveolar bone.
Phase of periodontal breakdown[bone loss].
All types of inflammatory cells.

22. Gingivitis cont’d…
22
Clinical Manifestations
Painful, inflamed, swollen gums
Usually the gums bleed in response to light contact or after
brushing
Development of pus
Formation of abscess with losing of teeth (periodontitis)

23. Complications of gingivitis
23
Abscess in the gingiva
Abscess in the jaw bones
Infection in the jaw bone or gingiva
Periodontitis - this is a more serious condition that can lead to
loss of teeth
Recurrent gingivitis
Trench mouth - ulceration of the gums caused by bacterial
infection

24. Gingivitis cont’d…
24
Treatment and Prevention
 Regular oral hygiene that includes daily brushing and flossing
 Professional cleaning of teeth
 Removal of the etiologic (causative) agent, plaque

25. Patient Education: Preventive Oral Hygiene
25
 Brush teeth using a soft toothbrush at least two times daily.
 Use an anti-plaque mouth rinse.
 Floss your teeth at least once a day
 Regularly rinse your mouth with an antiseptic mouthwash.
 Avoid smoking.
 Avoid refined sugars between meals
 Drink plenty of water
 Ensure adequate intake of vitamin C.
 Eat a balanced diet (avoid malnutrition)

26. Gingivitis cont’d…
26
 Visit a dentist at least every 6 months, or when you have a
chipped (cracked or broken) tooth, a lost filling, an oral sore that
persists longer than 2 weeks, or a toothache.
 Avoid alcohol and tobacco products.
 Maintain adequate nutrition and avoid sweets.
 Replace toothbrush at first signs of wear, usually every 2
months.

27. Periodontal disease
27
 Periodontal disease is destruction of bone and the
structures supporting the teeth.
 Periodontitis is irreversible, but you can stop its progression
through good oral hygiene and visiting your dental
professional

28. Warning Signs of Periodontal Disease:
28
 Gums that bleed when you brush or floss your teeth
 Gums that are red, swollen or tender
 Gums that have pulled away from teeth
 Infection including purulence (pus) between the teeth and gums when the
gums are pressed
 Permanent teeth that are loose or separating
 Any changes in the way your teeth fit together when you bite
 Any changes in the fit of your partial denture
 Bad breath
 Itchy sensation

29. EARLY AND MODERATE PERIODONTITIS:
29
 Periodontitis occurs when the inflammation of the gums
progresses into the deeper underlying structures and bone.
 In the most common form of Periodontitis, plaque (and
sometimes calculus) is found below the gum line.
 The gums may feel irritated, appear bright red, and bleed easily.
 The ligaments holding the tooth in its socket break down and the
gums pull away from the teeth, resulting in a periodontal pocket
or space between the tooth and gum.
 The periodontal pocket deepens and fills with more bacteria.
 Supportive ligaments and bone start to show damage.

30. Stomatitis
30
Is an inflammation of the mucous lining of the mouth
, which may involve the cheeks, gums ,tongue ,lips ,
and roof or floor of the mouth.
The word“ stomatitis “ literally means inflammation of
the mouth.
An inflammation of the mucous lining of any of the
structures in the mouth

31. Causes
31
Poor oral hygiene
Poorly fitted dentures
Mouth burns from hot food or drinks
Conditions that affect the entire body, such as
medications, allergic reactions, infections
Chronic irritation by tobacco—called Nicotine
stomatitis
Dietary deficiencies of iron
Chemotherapy & Radiotherapy
 Dehydration
•

32. Clinical manifestation
32
 Redness,
 Swelling,
 Bleeding (Occasional)
 Excessive salivation
 Halitosis
 Sore mouth

33. Managements
33
Removal or treatment of the cause,
Oral hygiene with soothing solutions is fundamental.
Topical medications
Soft bland diet
Correcting any vitamin B12, iron, or folate deficiencies

34. Disorders of the
Salivary Glands
34

35. Parotitis
35
 An inflammation of the parotid gland which are large salivary
glands located in front of each ear
Causative agents
 Bacterial infection of Staphylococcus aureus for adults
 Virus – epidemic (mump) for pediatrics

36. Parotitis cont’d…
36
Sign and symptoms
Pain of the gland and ear, fever
The gland swollen and becomes tense and tender
Swollen gland interferes swallowing,
Swelling increase rapidly and overlying skin soon becomes red and shiny

37. Parotitis cont’d…
37
Management
Maintaining adequate nutritional and fluid intake, good oral hygiene,
and discontinuing medications (e.g., tranquilizers, diuretics) that can
diminish salivation
Antibiotic therapy
Analgesics to control pain
If antibiotic therapy is not effective, the gland may need to be drained
by a surgical procedure known as parotidectomy.

38. Disorders of the
Esophagus
38

39. Achalasia
39
Absent or ineffective peristalsis of the smooth muscle layer of the
distal esophagus (the lower 2/3rd)-muscular ability to move food down
the esophagus
Accompanied by failure of the esophageal sphincter to relax in
response to swallowing
Also known as
 Esophageal achalasia
 Achalasia cardiae
 Cardiospasm
 Esophageal aperistalsis

40. 40
 Cause is unknown
Degeneration of nerve cells in muscular layer of esophagus
 Characterized by incomplete LES relaxation
 Aperistalsis of the esophagus in the absence of other explanations
like cancer or fibrosis
 People 40 years of age or older

41. Clinical Manifestations
41
 Difficulty in swallowing both liquids and solids
 A sensation of food sticking in the lower portion of the esophagus
 Food regurgitation
 Complaint of chest pain and heart burn (pyrosis)
 Secondary pulmonary complications

42. Diagnosis
42
 X-ray studies- show esophageal dilation above the narrowing at the
GEJ
 CT scan
 Endoscopy
 Barium swallow
 Manometry

43. Management
43
 Eating slowly and drinking fluids with meals
 Calcium channel blockers and nitrates- decrease esophageal
pressure and improve swallowing
 Injection of botulinum toxin- inhibit the contraction of smooth
muscle
 Balloon (pneumatic) dilation- stretch the narrowed area of the
esophagus
 Surgery: esophagomyotomy

44. Balloon (pneumatic) dilation
44

45. Hiatal Hernia/ hiatus hernia
45
 Normally, all of the stomach is below the diaphragm completely
being in the abdomen
 The muscle fibers in the diaphragm around the lower esophagus
help the sphincter to keep the esophagus closed to prevent
reflux of acid and food.
 It is the protrusion (or herniation) of the upper part of the
stomach into the thorax through a tear or weakness in the
diaphragm.
 It is also called diaphragmatic hernia or esophageal hernia.

46. Types of hiatal hernia
46
1. Sliding Hernia
 The upper stomach and the GEJ are displaced upward and slide
in and out of the thorax
 Is the most common type (90%)

47. 2. Paraesophageal Hernia
47
The GEJ remains fixed in its normal location and a pouch of
stomach is herniated (forming a pocket) beside the GEJ through
the esophageal hiatus

48. Etiology
48
 Actual cause not known
 Contributing factors
 Structural changes like
 Weakening of the muscles in
the diaphragm around the
GEJ
 Increased age, trauma
 Congenital weakness
 ed intrabdominal pressure
by:
 Obesity
 Pregnancy
 Ascites
 Tumors

49. Clinical manifestations
49
At least 50% of patients are asymptomatic
S/S may be similar to that of:
 GER
 Peptic ulcer and
 Angina
Heartburn/ burning pain
Regurgitation
Dysphagia
Reflux-- Sliding hiatal hernia
Feeling a sense of fullness after eating --paraesophageal hernia

50. Diagnosis
50
 Barium swallow
 Esophagoscopy with biopsy
 Ultrasonography
 X-ray studies
 Bronchoscopy

51. Management
51
A. Conservative management
 Frequent, small feedings
 Avoiding to recline for 1 hour after eating
 Elevating the head of the bed on 10 to 20cm blocks
 Antiacids and antisecretory agents
 Elimination of constricting garments
 Avoidance of lifting and straining
 Elimination of alcohol and smoking
 Weight reduction if the patient is obese

52. B. Surgical interventions
52
 Fundoplication
 Involves “wrapping” the fundus of the stomach around the lower
portion of the esophagus in varying degrees
Importance of the procedures
To reduce the hernia
 To provide an acceptable LES pressure
 To prevent the movement of the GEJ
360-degree wrap

53. 53
Partial anterior fundoplication Partial posterior fundoplication

54. Gastro-esophageal Reflux Disease (GERD)
54
 GERD is not a disease
 Is a syndrome produced by conditions that result in reflux
(back-flow) of gastric or duodenal secretions in to the
esophagus.
 The stomach lining protects the stomach from the effects of its
own acid but esophagus can’t protect itself producing S/S

55. GERD--Predisposing conditions
55
 Incompetent LES
 Conditions resulting in gastric
contents near the GEJ
 Bending down
 Hiatal hernia
 Decreased gastric emptying
 Certain drugs that interfere LES
function
  gastric pressure
 Dietary habits
Fatty foods
Chocolate
Caffeinated
Carbonated beverages
 Ingestion of alcohol
 Tobacco smoking
 Pyloric stenosis

56. Complications
56
 Esophageal irritation and inflammation
 Corrosion to the esophagus
 Scar tissue formation and decreased dispensability of secondary to
inflammation and irritation
 Aspiration

57. Clinical manifestations
57
 Pyrosis
 Dyspepsia (indigestion)
 Regurgitation
 Dysphagia
 Odynophagia
 Hypersalivation
 Esophagitis

58. Diagnosis
58
Barium swallow-determine if there is protrusion of the gastric
cardia
Esophagoscopy- determine the incompetence of the LES and
the extent of inflammation, potential scarring, and strictures
Biopsy and cytologic analysis
pH monitoring
Motility (manometry) studies
Bilirubin monitoring

59. Management
59
A. Patient education
 Low-fat diet
 To avoid caffeine, tobacco, beer, milk, foods containing
peppermint or spearmint, and carbonated beverages which
increase gastric secretion
 Eating or drinking 2 hours before bedtime
 To maintain normal body weight
 To avoid tight-fitting clothes
 To elevate the head of the bed on 15- to 20-cm blocks

60. GERD-- Mgt Cont’d…
60
B. Drugs
 Antacids- 1 to 2 hrs after meals and at bed time
 Histamine receptor blockers
 Proton pump inhibitors like omeprazole
 Cholinergics (e.g. bethanechol)
 Metoclopramide

61. 61
Gastritis

62. Gastritis Definition
62
 Is an inflammation of the gastric or stomach mucosa
 Is the result of a breakdown in the normal gastric barrier
(mucosa), which normally protects the stomach tissue from
auto-digestion by acid
Types
1. Acute Gastritis
2. Chronic Gastritis

63. Etiology --Acute Gastritis
63
 Drugs:
Steroidal & NSAIDs
 Alcohol
 Radiation
 Helicobacter pylori
 Staphylococcus organisms
 Bile and pancreatic secretions
 Physiology stress: shock, sepsis,
burns
 Psychologic stress
 Spicy, irritating foods
 Ingestion of strong acid or alkali
 Trauma: naso-gastric suction,
large hiatal hernia, endoscopic
techniques

64. Etiology-- Chronic Gastritis
64
 Repeated episodes of acute gastritis
 Benign or malignant ulcers of the stomach
 Bacteria helicobacter pylori
 Autoimmune diseases such as pernicious anemia
 Dietary factors such as caffeine
 Use of medications, like NSAIDs
 Chronic alcohol abuse
 Smoking
 Reflux of intestinal contents into the stomach

65. PP
65
Chronic Inflammation

chronic alterations in the protective mucosal barrier

Progressive gastric atrophy

Eventual death of chief and parietal cells

Decreased number of acid-secreting parietal cells

Hypochlorhydria Or
Achlorhydria

66. Clinical Manifestation
66
Acute gastritis
Anorexia, nausea and vomiting, hiccupping,
Epigastric tenderness
Feeling of fullness and abdominal discomfort
Hemorrhage associated with alcohol abuse
Headache, lassitude
Usually self-limited lasting from a few hours to a few days

67. C/Ms Cont’d…
67
Chronic gastritis
S/S are similar to that of acute gastritis
Anemia because of atrophy of cells producing intrinsic factor

68. Diagnosis
68
 Endoscopic examination with biopsy
 Complete blood count (CBC)
 Stool exam for occult blood
 Serologic test for H. pylori

69. Management
69
 The gastric mucosa is capable of repairing itself after a bout of
gastritis, in about 1 day
Acute Gastritis
Bed rest
Refraining from alcohol and food until symptoms subside
Parentral fluid—if symptoms persist
Neutralization
Antiacids like aluminum hydroxide -- if caused by ingestion of
strong acids
Diluted lemon juice or diluted vinegar --if caused by strong
alkali

70. Mgt Acute Gastritis Cont’d…
70
Antiemetis for nausea and vomiting
Antiacids
H2 antagonists
Blood transfusion and fluid replacement if gastritis is
hemorrhage

71. Mgt: Chronic Gastritis
71
Dietary & lifestyles modification
Reducing stress
Promoting rest
Initiating pharmacotherapy
 Antibiotics -- to treat H. pylori
 Proton pump inhibitor
 Bismuth salts
 Regular injections of VitB12—for patients with pernicious
anemia

72. Major Nursing Diagnoses
72
Imbalanced nutrition, less than body requirements, related to
inadequate intake of nutrients
Risk for imbalanced fluid volume related to insufficient fluid
intake and excessive fluid loss subsequent to vomiting
Deficient knowledge about dietary management and disease
process
Acute pain related to irritated stomach mucosa

73. Peptic Ulcer Disease
Gastric and Duodenal Ulcers
73

74. Definition
74
 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
 Ulcers are defined as breaks in the mucosal surface >5 mm in
size, with depth to the submucosa

75. Damage of gastric mucosa from irritants
75

76. Types of PUD
76
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)

77. Gastro-duodenal Mucosal Defense
77

78. Cause
78
 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
 Smoking

79. Cause Cont’d…
79
Ulcerogenic drugs
Tumors, like in case of Zollinger-Ellison syndrome (ZES)–
produce excessive amounts of the hormone gastrin
GERD- resulting esophageal ulcer
Familial tendency-genetic link– those with blood type O
Pregnancy appears to protect women from the developing ulcers

80. Pathophysiology
80
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

81. Clinical Manifestations
81
Symptoms may last for a few days, weeks, or months and may
disappear only to reappear, often without an identifiable cause

82. C/Ms Cont’d…
82
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 epigastrium
 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

83. C/Ms Cont’d…
83
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)
Epigastric tenderness
Abdominal distention

84. Emergency Complications
84
3 major emergency complications
1. Hemorrhage
2. Perforation
3. Gastric outlet obstruction

85. Complications Cont’d…
85
1. Hemorrhage
 Is the most common observed
 Cause
 Erosion of the ulcer through a major blood vessels

86. Complications Cont’d…
86
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

87. Complications Cont’d…
87
3. Gastric outlet obstruction
 Is the least common ulcer-related complication
 Cause
 Inflammation and edema in the peripyloric 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 the fills
and dilates
 May be relieved by belching or by self-induced vomiting

88. Complications Cont’d…
88
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

89. Duodenal vs Gastric Ulcers
89
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

90. GUs Vs DUs Cont’d…
90
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

91. Diagnosis
91
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

92. Management
92
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

93. Mgt Cont’d…
93
Conservative management/minimum medical treatments
Adequate rest
Dietary interventions
Medications
Elimination of smoking
Long-term follow-up care

94. Mgt Cont’d…
94
Lifestyle modifications
Adequate physical and emotional rest
A quite, calm environment
Elimination of stress
Moderate in daily activity

95. Mgt Cont’d…
95
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 may
irritate an inflamed mucosa
Proteins
 Best neutralizing food
 Stimulates HCl secretion
Carbohydrates and fats
 The least to stimulate HCl
secretion
 Don’t neutralize well

96. Nutritional Mgt Cont’d…
96
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

97. Mgt Cont’d…
97
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

98. Pharmacologic Mgt Cont’d…
98
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 system
Block the last step of acid production
Ex: Omeprazole, Lansoprazole, Rabeprazole

99. Pharmacologic Mgt Cont’d…
99
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

100. Pharmacologic Mgt Cont’d…
100
IV. Antibiotics for H. pylori
 Tetracycline + proton pump inhibitor + bismuth salts
 Amoxicillin + clarithromycin + proton pump inhibitor
 Metronidazole + clarithromycin + proton pump inhibitor
 Clarithromycin + proton pump inhibitor + amoxicillin

101. PUD Rx-- DACA-Ethiopia
101
I. PUD only
First Line
Ranitidine
150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks
Maintenance therapy: 150 mg at bedtime.
Alternatives
Cimetidine
400 mg P.O. BID, with breakfast and at night, OR
800 mg at night for 4 - 6 weeks
OR
Famotidine, 40 mg, P.O. at night for 4-6 weeks
OR
Omeprazole
20 mg P.O. QD for 4 weeks (DU) or 8 weeks (GU)

102. Pharmacologic Mgt Cont’d…
102
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
Amoxicillin, 1g, P.O. BID
PLUS
Metronidazole, 500mg, P.O. BID
PLUS
Omeprazole, 20mg P.O. BID OR 40mg QD for 7-14 days

103. Mgt Cont’d…
103
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

104. Mgt Cont’d…
104
3. Antrectomy- surgical removal, of antrum which is the lower
third of the stomach
 Antrum produces gastrin, which is a hormone that stimulates the production of
stomach acid
Removal of the lower portion of the antrum of the stomach as
well as a small portion of the duodenum and pylorus.
The remaining segment is anastomosed to the duodenum-
Gastroduodenostomy (Billroth I) or to the jejunum-
Gastrojejunostomy (Billroth II)

105. 105

106. Nursing Management
106
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

107. Nursing Interventions
107
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

108. Nsg Interventions Cont’d…
108
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

109. Nsg Interventions Cont’d…
109
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

110. Nsg Interventions Cont’d…
110
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

111. 111
Acute inflammatory
intestinal disorders

112. Appendicitis
112

113. Introduction
113
The Appendix
 A small, finger-like appendage about 10 cm (4 inch) long
 Attached to the cecum just below the ileocecal 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

114. Definition
114
 Appendicitis- is an inflammation of the vermiform appendix
Etiology
 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

115. PP
115
Obstruction

Distension

Venous engorgement

Accumulation of mucus and bacteria (pus)

Gangrene

Perforation

116. Clinical Manifestations
116
 Vague epigastric or periumbilical 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

117. 117

118. McBurney’s point and test of Rovsing’s sign
118

119. C/Ms Cont’d…
119
Signs
a. Rebound tenderness
b. Rovsing’s sign
Elicited by palpating the LLQ; this paradoxically causes pain
to be felt in the RLQ
c. Positive Psoas Sign
Feeling pain in the RLQ while applying resistance to the right
knee as the patient tries to lift the right thigh while lying down

120. Appendicitis-- Psoas Sign Cont’d…
120

121. C/Ms Cont’d…
121
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
Positive obturator sign
 Suggests irritation of the obturator muscle by an inflamed
appendix
If the appendix has ruptured
 The pain becomes more diffuse
 Abdominal distention develops
 The patient’s condition worsens

122. C/Ms Obturator Sign Cont’d…
122

123. C/Ms Cont’d…
123
 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.

124. Acute Complications
124
a. Perforation
 The most common and generally occurs 24 hours after the
onset of pain
b. Peritonitis
c. Abscess

125. Diagnosis
125
 History
 Complete physical examination
 Lab tests
CBC—ed WBCs (neutrophils >75%)
Serum electrolyte profile
 Abdominal x-ray films, ultrasound studies, and CT scans

126. Management
126
 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

127. 127

128. Nursing Management
128
Patient preparation for surgery
IV infusion to replace fluid loss and promote adequate renal
function
Antibiotic therapy to prevent infection
Enema is not administered
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

129. Nsg Mgt Cont’d…
129
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

130. Peritonitis
130
Peritoneum is:
 Double-layered, semipermeable
sac
 Lines the abdominal cavity and
covers some of the abdominal
organs
Peritoneal organs:
1.Liver
2.Stomach
3.Gallbladder
4.Spleen
5.Jejunum, ileum
6.Transverse and sigmoid colon
7.Cecum
8.Appendix

131. Definition
131
Is an inflammation of the peritoneum
Causes
The most common causative organisms:
Escherichia coli
Klebsiella
Proteus
Pseudomonas
Others organisims:
Streptococci spp
Staphylococci
Pneumococci

132. Cause Peritonitis Cont’d…
132
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

133. Clinical Manifestations
133
 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

134. C/Ms Cont’d…
134
 The affected area of the abdomen becomes extremely tender
and distended, and the muscles become rigid
 Ascites is found but virtually always predates infection
 Rebound tenderness
 Nausea and vomiting
 Peristalsis is diminished
 Increased temperature and pulse rate
 Almost always an elevated leukocyte count

135. Diagnosis
135
 Lab tests
 Increased leukocyte count
 ed Hemoglobin and hematocrit blood loss
 Serum electrolyte studies
 Abdominal x-ray- air or fluid level
 CT scan of the abdomen- abscess
 Peritoneal aspiration and culture

136. Complications
136
1. Sepsis-- the major cause of death
2. Shock bcs of septicemia or hypovolemia
3. Intestinal obstruction with bowel adhesion as a result of the
inflammatory process
4. Wound dehiscence and abscess formation
S/S
 Tender or painful abdomen
 Feeling as if something just gave way

137. Management
137
 Administration of several liters of an isotonic solution
 Analgesics
 Antiemetics
 Intestinal intubation and suction
 Oxygen therapy by nasal cannula or mask

138. Mgt Cont’d…
138
Large doses of IV broad-spectrum antibiotic until the specific
organism causing the infection is identified
Third-generation cephalosporins
Cefotaxime (2 g q8h, IV)
Ceftriaxone (2 g q24h IV)
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

139. Mgt Cont’d…
139
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)

140. Intestinal Obstruction
140

141. Intestinal Obstruction
141
 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

142. Types of Intestinal Obstruction Cont’d…
142
A. Mechanical Obstruction
Cause:
Intra-luminal obstruction or
Obstruction from pressure on the intestinal walls
Accounts for 90% of intestinal obstructions
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

143. Types of Intestinal Obstruction Cont’d…
143
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
 One part of the intestine slips into another part located below it
 Results in narrowing of intestinal lumen

144. Hernia (inguinal)
Intussusception
Types of Intestinal Obstruction Cont’d…
144

145. Types of Intestinal Obstruction Cont’d…
145
4. Volvulus
 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

146. Volvulus of the sigmoid colon
Types of Intestinal Obstruction Cont’d…
146

147. Types of Intestinal Obstruction Cont’d…
147
B. Functional Obstruction
 Intestinal musculature cannot propel the contents along the
bowel as result of neuromuscular or vascular disorders
Examples:
 Paralytic/adynamic ilues (the most common)
 Amyloidosis
 Muscular dystrophy
 Endocrine disorders such as diabetes mellitus
 Neurologic disorders such as Parkinson's disease

148. Small Intestine Obstruction
148
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

Increased capillary permeability

Circulating blood
Hypovolemic Shock
Edema, congestion, necrosis
Perforation of the intestinal wall
Peritonitis
Fluid and electrolyte extravasation to the peritoneal cavity

149. Clinical Manifestations
149
 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

150. C/Ms Cont’d…
150
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

151. Diagnosis
151
 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

152. Management
152
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

153. Nursing Management
153
Major Nursing Diagnoses May Include:
1. Pain related to abdominal distension and increased peristalsis
2. Fluid volume deficit related to decrease in intestinal fluid re-
absorption and loss of fluids secondary to vomiting
3. Altered nutrition: less than body requirements related to intestinal
obstruction and vomiting

154. Large Bowel Obstruction
154
Attributes to15% of intestinal obstructions
Commonly occur in the sigmoid colon
The most common causes:
Carcinoma
Diverticulitis
Impaction of feces
Benign tumors

155. Clinical Manifestations
155
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

156. Diagnosis
156
 History and physical examination
 Abdominal x-ray studies
 CT-scan
 Ultrasound
 Biopsy
 Laboratory studies
CBC
Serum electrolyte profile
 Barium enema
 To locate large intestinal obstruction
 Not used if perforation is suspected

157. Management
157
 Colonoscopy
Inspection of the interior surface of the colon
To untwist and decompress the bowel.
 Cecostomy
To make a surgical opening into the cecum for patients
 Who are poor surgical risks
 In need of urgent relief from the obstruction
 Temporary or permanent colostomy
 Ileoanal anastomosis
To remove the entire large colon
 Rectal tube
To decompress an area that is lower in the bowel

158. 158
Abdominal hernia

159. Abdominal hernia
159
 A protrusion of a biological tissue, structure, or part of an organ
through the muscular tissue or the biological membrane
Causes
 Condition that increases the pressure of the abdominal cavity
Obesity
Heavy lifting
Coughing
Straining
Fluid in abdominal cavity

160. Types of hernias
160
Inguinal hernia
 Most common hernias (up to 75%).
 For more understanding of inguinal hernias, much insight is
needed in the anatomy of the inguinal canal.
 Inguinal hernias divided into:
Indirect inguinal hernia
Direct inguinal hernia

161. Types of hernias cont’d…
161
Indirect inguinal hernia
Affects only men.
A loop of intestine passes down the canal from where a testis
descends early in childhood into the scrotum.
Increase progressively in size causing the scrotum to expand
grossly.
Direct inguinal hernia:
 Affects both sexes.
 The intestinal loop forms a swelling in the inner part of the fold of
the groin.

162. 162

163. Types of hernias cont’d…
163
Femoral hernia:
 Affects both sexes, although most often women.
 An intestinal loop passes down the canal containing the major blood
vessels to and from the leg.
Umbilical hernia
Umbilical hernias are especially common in infants
They involve protrusion of intra abdominal contents through a
weakness at the site of passage of the Umbilical cord.
These hernias often resolve spontaneously.

164. Types of hernias cont’d…
164
Incisional hernia
 Occurs when the defect is the result of an incompletely healed
surgical wound.
 These can be the most frustrating and difficult to treat, as the
repair utilizes already attenuated tissue.
Clinical manifestations
Pain and swelling

165. Hernia cont’d…
165
Complications
Inflammation
Bowel obstruction
Strangulation
Management
Repairing the weak abdomen part of abdominal wall.

166. 166
Diseases of the Anorectum

167. Diseases of the Ano-rectum
167
Patients seek medical care primarily because of
 Pain
 Rectal bleeding
 Change in bowel habits
 Protrusion of hemorrhoids
 Anal discharge
 Perianal itching and swelling
 Anal tenderness, stenosis, or ulceration

168. Anorectal Abscess
168
 Is undrained collection of perianal pus
 Caused by obstruction of an anal gland
 More prevalent in
 Immuno-compromised patients or
 Clients with inflammatory bowel disease (IBD)
 May occur in and around the rectum
 The most common causes are
 Escherichia coli
 Staphylococci
 Streptococci
 Many of these abscesses result in fistulas

169. Clinical Manifestations
169
Superficial abscess
 Local pain and swelling
 Redness
 Foul-smelling drainage
 Tenderness
Deeper abscess
 Lower abdominal pain
 Elevated temperature

170. Treatment
170
 Palliative therapy consisting of sitz baths and analgesics
 Incising and draining the abscess
 Packing the wound with gauze impregnated with petroleum
jell
 The packing should be changed every day
 Moist, hot compress application to the area
 Avoiding soiling the dressing during urination or defecation
 Patient education regarding wound care, sitz baths, thorough
cleaning after bowel movement, and follow up visit

171. Anal Fistula
171
 Is a tiny, tubular, fibrous tract/tunnel leading out from the anus or
rectum extending to:
 The outside of the skin
 Vagina
 Buttocks
 Usually precedes an anorectal abscess

172. Causes
172
 Inflammation/infection
 Trauma
 Fissures
Clinical Manifestations
 Leakage of stool or pus, blood stained drainage constantly
from the cutaneous opening
 Passage of flatus or feces from the vagina or bladder,
depending on the fistula tract
 Systemic infection in untreated fistulas

173. Management
173
 Wearing pad to prevent staining of cloth
 Fistulectomy
 An excision of the entire fistulous tract
 Packing the wound with gauze

174. Anal Fissure
174
 Is a longitudinal tear or ulceration in the lining of the anal canal
Cause
 Passing a large, firm stool
 Persistent tightening of the anal canal because of stress & anxiety
constipation
 Childbirth
 Trauma

175. Clinical Manifestations
175
Extremely painful defecation
Burning
Bleeding
Constipation as result fear of pain

176. Management
176
 Usually heals if treated by conservative measures
 Stool softeners and bulk agents
 An increase in water intake
 Sitz baths
 Emollient suppositories
 Suppository combined of an anesthetic with a corticosteroid
 Anal dilation under anesthesia
 Surgery, if fissures do not respond to conservative treatment

177. Hemorrhoids
177
 Hemorrhoidal vein: are veins draining the walls of the anal
canal and rectum
 Hemorrhoids are dilated portions of veins in the anal
canal and are very common conditions
Types
i. Internal hemorrhoids
Those above the internal sphincter
ii. External hemorrhoids
Appear outside the external sphincter
Occur at the anal opening and may hang outside the anus
By the age of 50, about 50% of people have hemorrhoids to
some extent

178. 178

179. 179

180. 180

181. Cause/Risk Factors
181
ed pressure in the hemorrhoidal tissue due to:
Pregnancy or giving birth
Strain during bowel movements
Holding back or waiting a long time before having a bowel
movement
Lifting heavy weights
Sitting for a long time on toilet
Overweight
Coughing or sneezing a lot
Sitting or standing for a long time
Having liver disease like cirrhosis

182. Clinical Manifestations
182
Common reasons for seeking health care:
 Bleeding
 Protrusion
 Anal itching
Anal ache or pain, especially while sitting
Pain during bowel movements

183. C/Ms Cont’d…
183
 External hemorrhoids are associated with severe pain
 Internal hemorrhoids are not usually painful until they bleed or
prolapse
 Bright red blood on toilet tissue, stool, or in the toilet bowl
 One or more hard tender lumps near the anus

184. Diagnosis
184
 History
 Physical examination
 Inspection of the perianal region
 Careful digital examination
 Anoscopy

185. Staging
185
The Staging of Hemorrhoids
Stage Description of Classification
I Enlargement with bleeding
II Protrusion with spontaneous
reduction
III Protrusion requiring manual
reduction
IV Irreducible protrusion

186. Management
186
 Relieving hemorrhoidal symptoms and discomfort
 Good personal hygiene
 Avoiding excessive straining during defecation
 High-residue diet that contains fruit and bran
 Increased fluid intake to soften stool
 Application of ice packs for a few hours, followed by warm
compresses
 Sitz baths
 Analgesic ointments and suppositories,

187. Mgt Cont’d…
187
 Bed rest
 T-binder to hold dressing in place
 Bismuth subgallate, insert one suppository in the rectum bid, or
use topical application, bid for five days
 Hemorrhoidectomy

188. 188
Management of Patients with
Hepatic Disorders

189. Hepatic Dysfunction
189
 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

190. The most common and significant symptoms of
liver disease
190
1. Jaundice
2. Portal hypertension, ascites, and varices
3. Nutritional deficiencies
4. Hepatic encephalopathy or coma

191. Jaundice/Icterus
191
Is yellowish-tinged or greenish-yellow discoloration of the body
tissues, including the sclerae, 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
Excretion of bilirubin into the biliary system

192. Types of Jaundice
192
1. Hemolytic
2. Hepatocellular
3. Obstructive

193. I. Hemolytic/ Prehepatic Jaundice
193
 Results from an increased destruction of the red blood cells
 Flood the plasma with unconjugated bilirubin so rapidly
Causes
 Hemolytic transfusion reactions
 Sickle cell crisis
 Hemolytic anemia

194. Bilirubin Metabolism
194

195. Hemolytic Jaundice Cont’d…
195
 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

196. II. Hepatocellular/ hepatic Jaundice
196
 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
Cirrhosis
 Patients may be mildly or severely ill

197. Hepato-cellular Jaundice Cont’d…
197
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

198. III. Obstructive / Posthepatic Jaundice
198
 Is due to impended or obstructed flow of bile
A. Intrahepatic 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
 Inflammatory exudate within the ducts themselves

199. Obstructive Jaundice Cont’d…
199
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

200. Obstructive Jaundice Cont’d…
200
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
Light or clay-colored stool
The skin may itch intensely
Intolerance to fatty foods

201. Obstructive Jaundice Cont’d…
201
Lab tests:
 AST, ALT levels generally rise only moderately,
 ed conjugated and unconjugated bilirubin
 ed urine bilirubin
 ed to no fecal or urinary urobilinogen

202. 202
Portal Hypertension

203. The Portal Venous System
203

204. Portal hypertension (PHpn)
204
Normal pressure in the portal vein is 5 to 10 mmHg
Obstructed blood flow via the damaged liver results in increased
blood pressure
PHpn is commonly associated with hepatic cirrhosis
It can also occur with noncirrhotic liver disease like thrombosis,
or clotting in the portal vein

205. 205
Alcoho 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
Hepatomegally
Splenomegaly
Jaundice
Ascites
BP
Esophageal varices
DHN

206. PHpn C/Ms
206
 GI bleeding/ Varices
 Spleenomegally
 Ascites
 Hepatic encephalopathy

207. Ascites
207
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

208. PP
208
Portal Hypertension/Resistance to Blood
Flow
Leakage of plasma into liver
lymphatics
Vasocongestion within
intestinal vasculature
Production of liver lymph with
high protein
Transudation of plasma into the
abdominal cavity
Leakage of lymph into
abdominal cavity with
osmotic gradient between
lymph & ECF
Ascites
Leakage of plasma out of
vascular space
 Intravascular oncotic pressure
 Albumin production
Hepatocyte Dysfunction

209. Clinical Manifestations
209
 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

210. 210

211. Assessing for abdominal fluid wave
211

212. Management of Ascites
212
Dietary Modification
Diuretics
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt

213. Esophageal Varices
213
 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 cirrhosis and varices

214. Factors that contribute to hemorrhage
214
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

215. Clinical manifestations
215
 Hematemesis
 Melena
 General deterioration in mental or physical status
 Symptoms of shock (cool clammy skin, hypotension, tachycardia)

216. Management
216
 Intravenous fluids with electrolytes
 Oxygen is administered to prevent hypoxemia/hypoxia
 Monitoring vital signs continuously
Pharmacologic Therapy
 Vasopressin (IV or intra-arterial)—to produce constriction of the
splanchnic arterial bed and resulting in decrease in portal pressure
 Propranolol and nadolol, beta-blocking agents that decrease portal
pressure
 Nitrates such as isosorbide- lower portal pressure by
vasodilation and decreased cardiac output

217. Endoscopic Sclerotherapy
217

218. Hepatic Cirrhosis
218
 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.

219. Types of cirrhosis or scarring of the liver:
219
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

220. Types of Cirrhosis Cont’d…
220
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
(cholangitis)
 Much less common

221. Clinical manifestation
221
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

222. Diagnosis
222
 History
 Physical Exam
 Diagnostic
Studies
 Liver scans/biopsy- Detects fatty infiltrates,
fibrosis, destruction of hepatic tissues, tumors
 Esophagogastroduodenoscopy (EGD)-
demonstrate presence of esophageal varices
 Electrolytes: Hypokalemia
 Urine urobilinogen: May/may not be present.
 Fecal urobilinogen: Decreased.

223. Dx
223
 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
 Increased Liver enzymes

224. Medical Management
224
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

225. Nursing Diagnoses may include:
225
1.Activity intolerance related to fatigue, general debility, muscle
wasting, and discomfort
2.Imbalanced nutrition, less than body requirements, related to
chronic gastritis, decreased GI motility, and anorexia
3.Impaired skin integrity related to compromised immunologic
status, edema, and poor nutrition
4.Fluid Volume excess related to compromised regulatory
mechanism (e.g., syndrome of inappropriate antidiuretic
hormone [SIADH], decreased plasma proteins, malnutrition) or
excess sodium/fluid intake evidenced by edema, anasarca,
weight gain
5.Knowledge, deficient regarding condition, prognosis, treatment,
self-care, and discharge

226. Hepatic Encephalopathy and Coma
226
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

227. Hepatic Encephalopathy cont’d…
227
 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

228. Hepatic Encephalopathy cont’d…
228
 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

229. Hepatic Encephalopathy cont’d…
229
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

230. Cholelithiasis
230
 It is the presence/formation of calculi in the gallbladder
 Usually form in the gallbladder from the solid constituents of
bile:
 Cholesterol
 Bile salts
 Bilirubin
 Calcium
 Protein
 They vary greatly in size, shape, and composition

231. 231

232. Types: there are two major types
232
A. Cholesterol stones
Predominantly composed of cholesterol
Is insoluble in water
Its solubility depends on bile acids and lecithin
(phospholipids) in bile
B. Pigment stones
Primarily composed of pigment
When unconjugated pigments in the bile precipitate to form
stone
Account for about one third of cases in the US
Cannot be dissolved and must be removed surgically

233. Risk factors
233
 Long –term parenteral nutrition, which results in decrease gal bladder
motility.
 Cirrhosis of the liver.
 Chronic hemolytic disorders, which result in increased bile pigments
 Obesity

234. Clinical Manifestations
234
 Gallstones may be silent
 Pain, tenderness, and rigidity of the upper right abdomen that
may radiate to the midsternal area or right shoulder
 Pain and biliary colic
 Bleeding tendency as a result of vitamin deficiency
 Changes in urine and stool color
 Very dark color urine
 The urine become foamy when shaken
 Clay-colored feces
 Jaundice

235. Management
235
Nutritional and supportive therapy
 Rest, intravenous fluids, nasogastric suction, analgesia, and
antibiotic agents
 Low-fat foods
 High protein and carbohydrates
 Cooked fruits, rice, lean meats, mashed potatoes, bread, coffee, or
tea may be taken
 Remind the patient that fatty foods may bring on an episode

236. Mgt Cont’d…
236
Pharmacologic therapy
Drugs to dissolve
 Ursodeoxycholic acid (UDCA)
 Chenodeoxycholic acid (chenodiol or CDCA)

237. Mgt Cont’d…
237
Non-surgical managements
 Dissolving gallstones by infusion of a solvent
 Lithotripsy- uses repeated shock waves directed at the gallstones
in the gallbladder
Surgical interventions
 Cholecystostomy
 Cholecystectomy
 Choledochostomy

238. Thanks for your
time &attention