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Mouth-Buccal/Oral Cavity
Saliva
• Produced by the salivary gland
• Moistens food to form bolus
• Dissolves food substances that begin chemical breakdown of starches
4. Teeth
• Used to chew (masticate)
• 32 permanent
• embedded at the gingiva
Pharynx
• Nasopharynx and oropharynx
• Provide passageway for food, fluids and air
• Its skeletal muscles move food to the esophagus (peristalsis)
• It has mucus producing glands that provide fluid for easy swallowing
Esophagus
• A muscular tube about 10 inches (25 cm)
• Serves as passageway of food
• Descends through the thorax and diaphragm
1. Epiglottis
• A flap of cartilage over the top of larynx
• Keeps food out of larynx during swallowing
Stomach
• Located high on the left side of the abdominal cavity
• A distensible organ – can hold up to 4 liters
• Regions:
a. cardiac region
b. fundus
c. body
d. pylorus
Functions:
1. Storage reservoir for food
2. Mechanical digestion
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3. Gastric glands has 4 cells:
a. Mucous
• Alkaline mucus
• Serves as protection against gastric juice
b. Zymogemic cells
• Pepsinogen (inactive pepsin-protein digesting enzyme)
c. Parietal
HCI
• Increases the activity of protein digesting cells
Intrinsic factor
• Absorption of vitamin B12
d. Enteroendocrine
• Gastrin, histamine, endorphirs, serotonin and sonatoslatin
• Gastrin- regulates secretion and motility of the stomach
Small Intestine
• Starts at pyloric sphincter and ends at ileocecal junction
• About 20 feet, one inch by diameter
• Divisions:
a. Duodenum
• Begins at the pyloric sphincter up to around the head of the pancreas
• Pancreatic enzymes and bile from the liver enter the small intestine
b. Jejunum - middle part
c. Ileum - terminal end of small intestine
• Site of chemical digestion and absorption through
a. microvilli
b. villi
c. circular folds
• Breaks carbohydrates and proteins
• Enzymes
a. Pancreatic amylase
• acts on starchy
b. Pancreatic enzymes
• breaks protein peptides
c. Pancreatic lipase
• breaks lipids
d. Triglycirides
• Enters as fat globules
• Coated by bile salts and emulsified
Functions:
1. Eliminates indigestible food residue
a. Goblet cells produce mucus- facilitates lubrication
b. Defecation reflex
• stretching of the rectal wall
• can be suppressed voluntarily
• expulsion can be attained by Valsalva maneuver
2. Absorbs water, salts and vitamins formed by the bacteria
Liver
• Largest gland
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• Approximately 3 pounds (1.4 kg)
• Located at the right side
• Made up of lobules (composed of plates of hepatocytes)
• Sinusoids
- blood filled spaces
- lined with Kaupffer cells (phagocytic cells)
Functions:
1. Secretes bile
2. Stores fat-soluble vitamins
3. Conjugates bilirubin
4. Stores blood and releases during hemorrhage
5. Synthesizes protein albumin
6. Synthesizes Prothrombin, Fibrinogen and factors I, II, VII, IX and X
7. Synthesizes fats from carbohydrates and protein energy or adipose tissue
8. Synthesizes cholesterol production of bile salts, steroid hormones and plasma membranes
9. Deamination (Amino acid carbohydrates)
10. Releases during hypoglycemia
11. Takes up glucose during hyperglycemia
12. Detoxification
13. Stores iron as ferritin (necessary for RBC production)
Pancreas
• Triangular gland extending across the abdomen
Functions
1. Produces 1-1.5 L of pancreatic juice everyday
2. Pancreatic juice
- clear with high bicarbonate content
- can digest all categories of food
INGESTION PROBLEMS
Etiology:
1. Mechanical = trauma
2. Chemical = irritants, drugs, toxins
3. Biological = infections
HS virus I & II
Spirochete
Bacteria - Staphylococcus, Streptococcus
4. Herpes Simplex:
Etiology: HS virus I & II
Also called “cold sore or Fever blisters”
Classified as STD
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S/S: Vesicles on an erythematous base; lesions @ junction of lips & face
Activated by: sunlight, heat, fever, menses, digestive disturbances, food allergies.
5. Vincent’s Angina
Known as “ Trench Mouth” / Acute necrotizing ulcerative gingivitis
Etiol: Fusiform bacteria, Spirochetes (Borrelia vincentii)
Purple-red gums with pseudomembrane
S/S: fever, anorexia, foul breath, cervical lymphadenopathy
Maybe acute, sub-acute or chronic
6. Aphthous Ulcer
Very painful, (1cm)
shallow erosions of called “canker sores”
circumscribe with white or yellow center, encircle by a red ring
8. Oral Candidiasis
Moniliasis or thrush
Etiol: prolonged high-dose antibiotic tx or steroids
S/S: Pearly, bluish-white milk curd membranous lesion at oral mucosa/larynx; sore mouth
yeasty halitosis
NDx1 = Pain:
Topical Xylocaine
Analgesics
Bland, Soft/liquid diet
Mild antiseptic mouthwash
ESOPHAGITIS
• Refers to herniation or displacement of a portion of the lower esophagus or the stomach into the
thoracic cavity.
Types:
1. Sliding esophageal hernia (90% of occurrences): herniated portion of the stomach slides back and
forth upward through the hiatus secondary to positional changes.
• weakening of the muscles of the esophageal hiatus due to the aging process (more than
60%)
• Trauma
• Hereditary factors
• Symptoms are associated with gastro-esophageal reflux:
1. Dysphagia
2. Pyrosis
3. Regurgitation
4. Bloating
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2. Rolling / paraesophageal esophageal hernia: fundus and possibly the greater curvature of the
stomach herniated alongside the esophagus into the thorax
• Occurs less commonly
• Complications are high and include gastric volvulus, strangulations, or obstruction.
• Symptoms are related to increased intrathoracic pressure:
1. Chest pain
2. Shortness of breath
3. Tachycardia with subsequent impaired gas exchange.
• Chest pain is characteristic because it mimics anginal pain and usually is not relieved when
the patient is recumbent.
Nursing Interventions:
1. Medications
Antacids
H2-receptor antagonists – Tagamet (Cimetidine)
Analgesics
2. Diet
Low-fat
Small frequent feedings
no alcohol, no caffeine, no spices
high-Fowler’s during and 1 hour eating
3. Advise patient to:
Reduce weight, if indicated
Avoid wearing tight-fitting or restricted clothing.
Alcohol and cigarette use.
4. Prepare for herniorrhapy / hernioplasty
Nissen Fuldoplicaion
GASTRITIS
B. Etiology
1. Acute (transient intermittent inflammation)
• Caused by:
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a. Local irritants (eg, drugs, alcohol, corrosive substances),
b. Allergy and bacterial endotoxin invasion (eg, Salmonella, Escherichia coli).
• Associated with mucosal hemorrhages and erosions.
2. Chronic gastritis
• Secondary to bile acid reflux or to peptic ulcer disease.
• Related to chronic use of local irritants (eg, alcohol, drugs)
D. Nursing Interventions
1. Correct fluid and electrolyte disorders.
2. Diet therapy.
3. Avoid oral feeding until emesis subsides.
4. Avoid foods contributing to gastric distress.
5. Parenteral therapy
6. Teach the patient about diet and lifestyle changes to prevent exacerbation.
7. Avoid cigarette smoking and alcohol consumption.
8. Medications:
a. Antacids
b. H2-receptor antagonist
A. Description
1. A chronic condition characterized by an ulceration of the gastric mucosa, duodenum, or less
frequently, of the lower esophagus and jejunum.
2. It is an acute response to medical or surgical stress.
1. Unknown
Infection (H. pylori) mucosal breakdown
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Genetic predisposition
Tobacco use
Ingestion of food or drugs that:
a. injure or alter gastric mucosa
b. increase hydrochloric acid production Stress
Diseases that alter gastric secretion (eg, pancreatitis, Crohn’s disease)
2. Duodenal ulcers are thought to occur more prevalent than gastric ulcers and usually occur between
the 2nd and 5th decades of life.
2. Duodenal ulcers.
1. Increased rate of gastric acid secretion (increased number of parietal cells or secondary to
vagal stimulation, affects gastric release.)
2. Dumping syndrome reduces the buffering effects of food.
3. Complications include hemorrhage, obstruction, or perforation.
3. Stress ulcers
1. Coffee ground aspirate - hallmark sign
2. Multiple ulcerations felt to be erosions develop secondary to gastric ischemia.
4. S/Sx common to all PUDs:
1. Bloating
2. Belching
3. Nausea
4. Vomiting
5. Pain (usually described as burning or aching)
a. Gastric – relieved by eating
b. Duodenal – aggravated by eating
6. Pain may be associated with:
a. ingestion of specific foods (spicy or fried)
b. Alcohol
c. medications
D. Medical Management
1. Medications
a. Antacids
• Neutralizes HCl
• Taken 1-2 hours pc
• Examples: Amphogel (AL-OH), Basaljel (AL-Carbonate), Milk of Magnesia (Mg-PH), Maalox
(AL-MG-OH)
• Magnesium-based diarrhea
• Aluminum-based constipation
b. H2 receptor antagonists
• Reduces HCl secretion
• Taken with meals
• Examples: Tagamet (Cimetidine), Zantac (Ranitidine)
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• Side effects:
Diarrhea
Abdominal cramps
Confusion
Dizziness
Weakness
c. Cytoprotective drugs
• Coats ulcer
• Taken on an empty stomach (30-60 mins ac)
• Example: Carafate (Sucralfate)
2. Surgeries
b. Vagotomy
• Resection of the vagus nerve
• Decreases cholinergic stimulation decreases HCL secretion
c. Pyroplasty – surgical dilatation of the pyloric sphincter
d. Antrectomy
• Billroth I
• Billroth II
• Subtotal Gastrectomy
o Removal of 75% of the distal stomach
E. Nursing Interventions
1. Relieve pain: Take prescribed medications as ordered
2. Promote a healthy lifestyle
a. Diet
1. Liberal bland diet during exacerbation
2. Eat slowly and chew food properly
3. Small, frequent feedings during exacerbation
4. Avoid the following:
a. Fatty foods
b. Coffee, tea, cola drinks, chocolate
c. Spices, red /black pepper
d. Alcohol
e. Bedtime snacks
f. Binge eating
g. Large quantities of milk (400 mls/day is allowed)
b. Quit smoking
c. Coping
• Stress Therapy
(a) Recreation and hobbies
(b) Regular pattern of exercise
(c) Stress reduction at home and at work
GASTROENTERITIS
A. Description
1. Is an inflammation of the GI; it most commonly affects the small intestine.
2. A.K.A Traveler’s diarrhea, dysentery.
3. History – will differentiate from other conditions
D. Nursing Intervention
1. Drugs – anti-infective agents, analgesics, and electrolyte replacement medications (eg,
potassium). No drugs to suppress gastric motility.
2. Monitor I & O
3. Watch out for F & E imbalances
4. Dietary changes
• intake of clear liquids initially
• lactose-free foods for 1 to 2 weeks (after symptoms subside)
5. Parenteral therapy for severe cases.
6. Collect stool specimen.
7. Provide meticulous perianal skin care.
8. Provide patient teaching covering:
• Adherence to medication regimen
• Appropriate sanitary methods for cooking and personal hygiene
ULCERATIVE COLITIS
A. Description: Is an inflammatory process affecting the mucosa of the colon and rectum.
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D. Overview of Nursing Interventions
1. Administer medications, as ordered.
a. Antimicrobial c. Antidiarrheal
b. Antispasmodics
2. Institute dietary management:
a. Low-residue c. Elemental type (fast GI absorption)
b. Lactose-free d. TPN if needed
3. Monitor I & O
4. Collect stool specimen
5. Monitor weight
6. Prepare for surgery and institute postoperative care.
A. Description
1. Chronic inflammatory bowel disease affecting segmental areas along the entire wall of the GI
tract.
B. Etiology
1. Exact cause unknown; usually associated with:
a. Infectious process
b. Allergy or autoimmune disorders
c. Genetic predispositions
DIVERTICULITIS
A. Description: An inflammation of the diverticula or herniations within the wall of the intestinal tract.
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D. Overview of Nursing Interventions
Everyday life:
1. Administer antimicrobial agents as ordered.
2. Bulk-forming laxatives
3. Dietary regimen:
a. Low fiber diet
b. Eliminate foods with seeds and nuts.
4. Encourage fluid intake
5. Observe fluid status and bowel movement.
6. Prepare for colostomy; institute postoperative care.
APPENDICITIS
A. Description: Is the inflammation of the vermiform appendix.
B. Etiology:
1. Exact cause is unknown. Factors may include:
a. Fecal impaction
b. Kinking of the appendix
c. Parasites
d. Infections
PANCREATITIS
B. Etiology: Results from alterations in the structure or function of the pancreas, commonly caused by
chronic alcohol abuse.
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C. Pathophysiology and manifestations
Peritonitis
Neurogenic shock Necrosis
HEMORRHOIDS
• Dilated blood vessels beneath the lining of the skin in the anal canal
• Two Types of Hemorrhoids
– External hemorrhoids – occur below the anal sphincter
– Internal hemorrhoids – occur above the anal sphincter
• Causes
– Chronic constipation
– Pregnancy
– Obesity
– Prolonged sitting or standing
– Wearing constricting clothings
– Disease conditions like liver cirrhosis, RSCHF
Collaborative Management:
1. High fiber diet, liberal fluid intake
2. Bulk laxatives
3. Hot Sitz bath, warm compress
4. Local anesthetic application – Nupercaine
5. Surgery
• Hemorrhoidectomy
• Sclerotherapy (5% phenol in oil)
• Cryosurgery
• Rubber – band ligation
6. Preop Care
• Low residue diet to reduce the bulk of stool
• Stool softeners
7. Postop Care
a. Promotion of comfort
• Analgesics as prescribed
• Side – lying position
• Hot Sitz bath 12 to 24 hrs. postop
b. Promotion of elimination
• Stool softener as prescribed
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• Encourage the client to defecate as soon as the urge occurs
• Analgesic before initial defecation
• Enema as prescribed, using a small – bore rectal tube
c. Patient Teaching
• Clean rectal area thoroughly after each defecation
• Sitz bath at home especially after defecation
• Avoid constipation:
o High – fiber diet
o High fluid intake
o Regular exercise
o Regular time for defecation
• Use stool softener until healing is complete
• Notify physician for the following:
o Rectal bleeding
o Continued pain on defecation
o Continued constipation
LIVER CIRRHOSIS
Types:
1. Laennec’s cirrhosis – the most common
1. Caused by the liver’s toxic to alcohol
2. Occurs primarily in middle-aged men
2. Postnecrotic cirrhosis
1. Results from severe liver disease
2. Post - acute viral or chemical hepatitis
3. Primary biliary cirrhosis: inflammation and intrahepatic bile duct destruction.
4. Secondary biliary cirrhosis: chronic partial or complete common bile duct obstruction due to gall
stones, pancreatitis or tumor.
5. Cardiac cirrhosis results from right-sided CHF.
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Enlarged liver congested venous blood flow failure of the heart to pump blood to different
areas of the body.
Congestion causes anoxia to the liver necrosis and fibrosis
Hepatorenal syndrome
A major complication of cirrhosis
characterized by renal failure in an anatomically normal kidneys progressive oliguria and
azotemia.
Nursing Interventions:
1. Assess for signs of bleeding
2. Monitor V/S and laboratory results (platelets, creatininine)
3. Monitor I/O.
4. Monitor daily weight and abdominal girth to detect ascites.
5. Administer the following as ordered to combat symptoms:
1. Vitamin K
2. Stool softeners
3. Diuretics
6. Assess for changes in cardiac output, decreased renal function and electrolyte imbalances.
7. Assess for impaired skin integrity related to edema, ascites and pruritus.
8. Use preventive measures to keep skin intact.
9. Assess the patient for signs of impaired breathing related to congestion or infection.
10. Relieve breathing difficulty.
11. Observe for signs of encephalopathy (lethargy, confusion, personality changes, motor changes,
depression, irritability).
12. Teach ways to decrease bleeding tendencies.
14. Patient teaching:
a. Nutritional needs
b. Avoidance of alcohol
c. Drug interactions related to decreased liver function.
d. Enough rest
e. Signs and symptoms needing medical intervention.
15. Provide counseling for the patient and family.
CHOLELITHIASIS/CHOLECYSTITIS
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• poor absorption of fat soluble vitamins
4. Increased serum bilirubin
• Jaundice
• Pruritus
• Tea-colored urine
5. Infection
• Cholecystitis
• Pancreatitis
Management:
1. Relief of pain
• Meperidine HCL, not MorphineSO4
2. Diet: low fat diet
3. Bile salts: chenodeoxycholic acid, ursodioxycholic acid given after meals
4. Surgery: cholecystectomy
Preop care:
1. IVF to replace loss in vomiting
2. DBCT
3. Vit K injection
Postop Care
1. Low or semi-fowler’s position
2. NGT for decompression
3. Diet: low fat for 2-3 months
4. Ambulation after 24 hrs post op
5. T tube if with CBD exploration
• Purpose is to drain bile
• Drainage:
o Brownish red for 1st 24 hrs
o 300-500 ml of bile drainage for 1st 24 hrs
o Drainage bottle should be placed in bed at level of incision to drain excess but not all of
the bile
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