upper GI tract disorders

HERNIA
I. Sliding Hiatal Hernia
• protrusion of the esophagogastric junction into the thoracic cavity
• causes: muscle weakness in the esophageal hiatus
aging process
obesity
trauma
surgery
prolonged intra-abdominal pressure

II. Paraesophageal/Rolling Hernia

• Gastric junction remains below the diaphragm, but fundus of the stomach and
the greater curvature rolls into the thorax
• Cause: anatomic defect

CLINICAL MANIFESTATIONS
Heart burn
Dysphagia/odynophagia
Dyspnea
Abdominal pain
Nausea/vomiting
Gastric distention, belching, flatulence (rolling hernia)

MANAGEMENT
• pharmacologic therapy
Antacids (H2 receptor blockers, proton pump inhibitors)
Antiemetics
AVOID: Anticholinergics
Xanthine derivatives
Ca-channel blockers
Diazepam

• Nursing interventions
1. relieve pain
Modify diet
2. high CHON diet to enhance LES pressure
Small frequent feedings
Eat slowly and chew food properly
AVOID: fatty foods, cola beverages, coffee, chocolate, alcohol
Assume upright position before and after eating (1-2 hours)
Do not eat at least 3hours before bedtime; No evening snacks
Reduce BW if obese
3. promote lifestyle changes
Elevate head of bed to 12 inches for sleep
AVOID instances that increase intra-abdominal pressure
constrictive clothing
 straining
heavy lifting
bending, stooping
excessive coughing

GASTRO-ESOPHAGEAL REFLUX disease (GERD)

• Backflow of gastric content into the esophagus

CLINICAL MANIFESTATIONS
Heartburn
Dyspepsia
Regurgitation
Epigastric pain (esophagitis)
Odynophagia
Ptyalism

DIAGNOSTIC TEST
Endoscopy or barium swallow
Gastric ambulatory pH analysis (notes pH of the esophagus; done for 12-36
hrs)

NURSING INTERVENTIONS
1. instruct client to AVOID stimuli that ↑↑ stomach pressure and ↓↓ GES
pressure
2. instruct to AVOID spices, coffee, tobacco and carbonated drinks
3. Instruct on LOW FAT, HIGH FIBER diet
4. AVOID intake of foods and drinks TWO hours before bedtime
5. AVOID tight-fitting clothes
6. elevate the head of bed ~ 8 inches high
7. administer medications (H2 blockers, PPI)

SURGICAL INTERVENTION
~~ Nissen Fundoplication (Gastric wrap-around) to tighten GES
Monitor: persistent dysphagia and gas pain post-op

BARRETT’S ESOPHAGUS
- Sequelae of long-standing GERD
- Esophageal lining is altered (stratified squamous to columnar)
- Precursor to esophageal Ca
- Esophagus appears red rather than pink
- Prophylactic transhiatal esophagectomy

GASTRITIS
• Inflammatory condition causing breakdown of the normal gastric protective
barriers with subsequent diffusion of HCL into the gastric lumen

ACUTE GASTRITIS
Secondary to dietary indiscretion, medications, alcohol

CHRONIC GASTRITIS
Type A - associated c autoimmune, atrophic gastritis, pernicious anemia,
achlorhydria
- Caused by antibodies destroying the parietal cells and intrinsic factor
leading to low gastric acid levels

Type B – caused by H. pylori

- associated with increased gastric acid secretion

• ETIOLOGY
Chronic ingestion of irritating foods (highly seasoned, contaminated foods)
ROH, NSAIDs

• CLINICAL MANIFESTATION
h/a, n/v,
abdominal discomfort
hiccupping (hours to days)
heartburn after eating
belching
food intolerances

• PATHOPHYSIOLOGY
Inflammation
Edema; hyperemia
Superficial erosion
↓↓ gastric juice (↓ acid; ↑mucus) =
achlorhydria
Further erosion of gastric
mucosa

• MEDICAL MANAGEMENT

1. eliminate cause ( XXX ROH, foods till s/sx subside)

2. antacids as ordered
3. monitor and maintain fluid and electrolyte balance
4. AVOID coffee, spicy foods, alcohol, NSAIDs, steroids

• SURGICAL INTERVENTION
Gastric resection/ gastrojejunostomy
PEPTIC ULCER DISEASE

• Circumscribed lesions in the mucosal membranes of the stomach (gastric ulcer)

and duodenum (duodenal ulcer)

• PRECIPITATING FACTORS
Decreased mucosal resistance
Defective mucus secretions
Helicobacter pylori
Prolonged NSAID and steroid use
Inadequate mucosal blood flow
Acid hypersecretion
Cigarette smoking
Stress

~~ Zollinger-Ellison Syndrome
Ulcer resistant to medical therapy
Severe peptic ulcer
Extreme gastric hyperacidity
Gastrin-secreting benign/malignant pancreatic tumor

Duodenal ulcer Gastric ulcer

commonly in the first 2cm of the
duodenum
H. pylori, ROH, smoking, stress
Pain occurs 1-3 hrs pc, wakes up at
midnight to 3am
Pain in mid-epigastrium (burning,
cramping)
High gastric acid levels
Relieved by food, antacids and H2
blockers
Not associated with vomiting
Does not represent malignancy
Usually not accompanied by
complication
Melena> hematemesis
Most commonly found in the antrum
H. pylori, ROH, smoking stress, NSAID
Pain occurs within a short time pc
Low to normal gastric acid levels
Pain in the upper left epigastrium with
possible radiation to the back
Pain may be exacerbated by food
Accompanied by n/v (relieves pain) = wt
loss
Malignancy is most likely
Accompanied by bleeding, higher
mortality (hematemesis>melena)

• NURSING INTERVENTION
1.WOF s/e of cimetidine: dizziness, rash, mild diarrhea
2. health teaching
a. medication regimen
take medication at prescribed time (antacids are taken one hour AFTER
meals)
have antacids available at all times
b. proper diet
BLAND DIET consisting of six SMALL MEALS per day.
Eat meals slowly
AVOID caffeine, ROH, highly seasoned foods, nicotine, milk/creams
AVOID stressful situations
 c. prepare for surgery (usually indicated for ulcers not healing for 12-16wks

• MEDICAL MANAGEMENT
1. supportive: rest, diet, stress management
2. drug therapy
H2 receptor antagonist, PPI (to decrease HCL secretion)
Anticholinergics (to decrease gastric juice secretion)
Antibiotics (eradicate H. pylori)
Recommended Therapy: 10-14days
Triple therapy – 2 antibiotics + PPI
Quadruple therapy – 2 antibiotics + PPI + bismuth salt
3. surgery

a. Vagotomy: severing of part of the vagus nerve innervating the stomach to

decrease gastric acid secretion
b. Pyloroplasty: enlargement of the pyloric sphincter with acceleration of gastric
emptying
c. Antrectomy: removal of the antrum of the stomach to eliminate the gastric
phase of digestion
Gastroduodenostomy (Bilroth I): removal of the lower portion of the
stomach with anastomosis of the remaining portion of the duodenum

Gastrojejunostomy (Bilroth II) removal of the antrum and distal portion

of the stomach and duodenum with anastomosis of the remaining portion of the
stomach to the jejunum

d. Gastrectomy: removal of 60-80% of the stomach

e. esophagojejunostomy (total gastrectomy): removal of the entire stomach
with a loop of jejunum anastomosed to the esophagus

Nursing Intervention post-operative

1. routine post-op care
2. ensure adequate function of the NGT
anticipate frank, red bleeding for 12-24 hours
do not manipulate the tube and ensure its patency
3. promote adequate ventilation
4. promote nutrition
- After removal of NGT, provide clear liquids with gradual introduction of
small amounts of bland food at frequent intervals
- Gradually increase food intake until able to tolerate usual meals
5. manage complication
- AVOID concentrated sweets.
- LOW CHO, HIGH CHON, moderate fats
- Adhere to six small meals per day
- refrain from taking fluids during meals but rather 2hrs after meals
- assume recumbent position for ½ hrs after meals
DUMPING SYNDROME

• Unpleasant vasomotor and GI symptoms caused by rapid emptying of gastric

content into the jejunum

Early signs and symptoms (5-30 minutes pc)

Rapid emptying of hypertonic food from the stomach

↓↓
Distention of the jejunum (feeling of fullness)
↓↓
Fluid shift from bloodstream into jejunum
↓↓
Decreased blood volume
↓↓
Shock-like manifestations
(weakness, tachycardia, dizziness, diaphoresis, nausea explosive
diarrhea)

Late signs and symptoms (2-3 hours pc)

Sudden hyperglycemia
↓↓
Increased insulin secretion
↓↓
Rebound hypoglycemia (50mg/dl)
( faintness)

MANAGEMENT
1. eat in recumbent or semi-recumbent position
2. Lie down after a meal (LEFT side)
3. Small, frequent feedings
4. MODERATE FATS, HIGH PROTEIN diet (fats slow down gastric motility increasing
colloidal
osmotic pressure and prevents shifting of plasma)
5. limit CHO, NO simple sugars
6. give fluids few hours after meals or in between meals
7. AVOID very HOT or COLD foods and beverages
8. anticholinergics or antispasmodics are given
lower gi tract disorders

INTESTINAL OBSTRUCTION

• physical blockage of the passage of intestinal contents with subsequent

distention by fluid and gas
• ETIOLOGY: adhesions, hernias, volvulus, intussusceptions, inflammatory bowel
disease, foreign bodies, strictures, neoplasms, fecal impaction

PARALYTIC ILEUS: interference with the nerve supply to the intestine resulting in
decreased or absent peristalsis

VASCULAR OBSTRUCTIONS: interference with the blood supply to apportion of the

intestine resulting in ischemia and gangrene of the bowel

CLINICAL MANIFESTATION
1. small intestine: non-fecal vomiting colicky intermittent abdominal pain
2. large intestine: cramplike abdominal pain, occasional fecal vomitus; client is
unable to pass stools or flatus
3. abdominal distention, rigidity, high pitched bowel sounds above the level of the
obstruction, decreased or absent bowel sounds distal to the obstruction

DIAGNOSTIC TESTS AND FINDINGS

1. flat-plate (x-ray) of the abdomen – presence of gas and fluid
2. HCT increased
3. serum NA+, K+, Cl- decreased
4. BUN increased

NURSING INTERVENTION
1. monitor fluid and electrolyte balance, prevent further imbalance: keep on NPO
nd administer IV fluids as ordered
2. accurately measure drainage from NGT
3. place client in FOWLER’s position to alleviate pressure on diaphragm
encourage nasal breathing to minimize swallowing of air and further abdominal
distention
4. institute comfort measures associated with NG intubation and intestinal
decompression
5. measure abdominal girth daily
Assess for signs of peritonitis
Monitor UO
INFLAMMATORY BOWEL DISEASES (IDIOPATHIC INFLAMMATORY BOWEL DSE)

Crohn’s Disease
Inflammatory reaction
Terminal ileum thickens
scarring, ulcerations
abscess formation
narrowing of the lumen

Ulcerative Colitis
Inflammatory reaction
Edema of the affected segment
Development of bleeding ulcers
Scarring (over time) – loss of elasticity
Impaired water absorption

CROHNS DISEASE (Regional Enteritis) ULCERATIVE COLITIS

Assessment Assessment
Fever Fever
Abdominal distention Abdominal pain and cramping
Bloody diarrhea Severe diarrhea with rectal bleeding
Colicky abdominal pain
Anorexia, n/v Anorexia
Weight loss Weight loss, Dehydration
Anemia Anemia
Pathology
Transmural thickening Mucous ulceration; shortening of
Regional, segmental colon
Narrowing of the colon Diffused involvement of the colon
Mucosal edema (-)
(-)
Location
Ileum, Ascending colon Rectum/ descending colon, sigmoid
Etiology unknown
Predisposition
Jewish Jewish; Caucasian
Environmental Familial
Emotional stress
20-30y/o; 40-60 y/o 15-40 y/o
Bleeding
Low episodes; stool with pus and Severe; stool with blood
mucus
Perianal involvement
 Severe, common Mild
Fistulas
Common Rare
Rectal involvement
20% 100%
Diarrhea
5-6 soft stool/day 20-30 watery stool/ day
Abdominal pain (+) (+)
Weight loss (+) (+)
Intervention
TPN TPN; diet
Steroids Steroids
Azulfidine (Sulfasalazine) Azulfidine (Sulfasalazine)
Ileostomy Ileostomy
Colectomy Proctocolectomy

MANAGEMENT
Goal: rest the bowel and decrease diarrhea

1. maintain NPO during the active phase

2. monitor for complications: severe bleeding, dehydration, electrolyte imbalance
3. monitor for bowel sounds, stool and blood studies
4. restrict activities
5. administer IVF, electrolytes and TPN as prescribed
6. AVOID: GAS-FORMING FOODS MILK PRODUCTS
WHOLE GRAINS & NUTS RAW fruits and vegetables
PEPPER ALCOHOL
CAFFEINE
7. DIET PROGRESSION: clear liquid – LOW residue, HIGH protein diet
8. administer meds as ordered:
anti-inflammatory antibiotics steroids
bulk-forming agents vitamin/Fe supplements
9. colostomy, ileostomy

DIVERTICULITIS/DIVERTICULOSIS
• DIVERTICULUM – outpouching of the mucosal lining of the GIT (colon)
• DIVERTICULA/DIVERTICULOSIS – multiple outpouchings
• DIVERTICULITIS – acute inflammation and infection caused by trapped fecal
material and bacteria
• ETIOLOGY:
low fiber diet chronic constipation obesity

• PATHOPHYSIOLOGY
Increased intramural pressure (valsalva maneuver, constipation)
Decreased muscle strength in the colon wall
Herniation/ outpouching of the mucus membrane
 Entrapment of fecal material and bacteria
Inflammation and infection
Scarring

CLINICAL MANIFESTATION

1. dull, steady, cramplike LLQ pain that worsens with movement, coughing or
straining
2. low-grade fever
3. chronic constipation with episodes of diarrhea
4. n/v
5. abdominal distention ad tenderness
6. occult bleeding, rectal bleeding, change in bower movement
7. signs and symptoms of peritonitis (due to perforation and development of
abscess)

~~ Barium enema is not ordered because of the possibility of perforation

NURSING MANAGEMENT
1. high fiber diet
2. liberal liquid intake of 1500 -300ml/day
3. AVOID nuts and seeds which can become trapped in the diverticula
4. bulk-forming laxatives are ordered to restore normal bowel pattern
5. during an acute episode:
Bedrest
NPO then clear liquid to rest bowel
AVOID high fiber foods to prevent further irritation of the mucosa
IVF and medications: antibiotics, narcotic analgesics, anticholinergics,
antispasmodics
NGT to relieve obstruction
Weight loss to reduce intra-abdominal pressure
6. encourage daily walking, exercise and weight reduction

APPENDICITIS

• inflammation of the vermiform appendix that prevent mucus from passing into
the cecum; if untreated, ischemia, gangrene, rupture, and peritonitis occur
• ETIOLOGY: mechanical obstruction (fecalith, intestinal parasites, kinking of
appendix, tumor or inflammation), anatomic defect
• PATHOPHYSOLOGY
Obstruction of the appendix lumen
Mucosal inflammation and bacterial proliferation
Increased intraluminal pressure
Lymphoid swelling
Decreased venous drainage
Thrombosis
Bacterial invasion
 Abscess formation
Gangrene
Perforation(24-36hrs)
Peritonitis

• CLINICAL MANIFESTATION

1. Acute abdominal pain that usually starts in the epigastric or umbilical region
Pain gradually becomes localized in the RLQ/Mc Burney’s point
Pain is initially intermittent then becomes steady and severe over a short
period
2. Appendicitis ‘signs’
Blumberg sign – rebound tenderness
Psoas sign – lateral position with right hip flexion
Rovsing’s sign – LRQ pain when left if palpated
Obturator sign – pain on external rotation of the right thigh
3. sudden decrease of pain followed by a progressive distention, rigid
abdomen and unrelenting pan may signal perforation/rupture of the appendix
4. n/v and anorexia
5. guarding of abdomen, walks stooped over “AP walk”
6. decreased bowel sounds
7. low grade fever (T=38-38.5). high grade for ruptured appendix
8. diagnostic findings:
elevated WBC (> 10,000/cu mm)
elevated acetone in urine
UTZ and abdominal x-ray to detect the fecalith

• MANAGEMENT
1. bed rest
2. NPO
3. relieve pain (cold application over the abdomen, NEVER heat)
4. AVOID factors that increase peristalsis
Heat application over the abdomen
Laxative
Enema
5. IVF therapy to maintain fluid-electrolyte balance
6. antibiotic therapy
7. surgery: appendectomy

Surgical procedure
Spinal anesthesia
Flat on bed 6-8hrs Post-operative
Monitor for return of sensation in the lower extremities
NPO until peristalsis returns
Ambulation after 24 hrs
If ruptured (peritonitis) with penrose drains, Position on semi fowler’s to
localize
inflammation within the pelvic cavity
 Monitor NGT output
Administer antibiotics as ordered
Resume all normal activities within 2-4 weeks

HEMORRHOIDS

• Dilated blood vessels beneath the lining of the skin in the anal canal
• Types:
o External hemorrhoids – below the anal sphincter
o Internal hemorrhoids – above the anal sphincter
o mixed
• Causes:
o Chronic constipation – straining Pregnancy – after vaginal
delivery
o Obesity – ↑↑ intraluminal pressure Prolonged sitting or standing
o Wearing constricting clothing Disease conditions – liver cirrhosis,
RSCHF

• CLINICAL MANIFESTATIONS
o Constipation in an effort to prevent pain or bleeding associated with
defecation
o Anal pain and itchiness
o Rectal bleeding usually bright red hematochezia
o Mucous secretion from the anus
o Sensation of incomplete evacuation of the rectum
o Internal hemorrhoids may prolapse usually painless (external
hemorrhoids are usually painful due to vascular congestion)

• MANAGEMENT
o High fiber diet, liberal fluid intake Bulk laxatives
o Hot sitz bath, warm compress Local anesthetic application –
Nupercaine

• SURGERY
o Hemorrhoidectomy
o Sclerotherapy
o Cryosurgery – extreme cold to freeze and destroy unwanted tissue
o Rubber-band ligation - done only in INTERNAL hemorrhoids
Pre-op care: low residue diet to reduce bulk of stool
Stool softeners
Post-op care: promotion of comfort Analgesics
Position: lateral or prone
Hot sitz bath 12-24 hrs post-op
Promotion of elimination
Stools softeners are given as prescribed till complete
healing
 Analgesics before initial defecation
Encourage defecate as soon as urge occurs
Patient teaching
Sitz bath after defecation
Avoid constipation
High fiber diet, OFI
Regular exercise and time for defecation
Notify physician for: Rectal bleeding & excessive
drainage
Continued pain on defecation &
constipation