Exam 2: GI Disorders Flashcards
Hiatal Hernia
Protrusion of a portion of the stomach into the esophagus through an opening or hiatus in the diaphragm.
Types of Hiatal Hernia
- Sliding Hiatal Hernia
2. Paraesophageal or rolling Hiatal Hernia
Sliding Hiatal Hernia
When the stomach slides into the thoracic cavity when in supine position and slides back into the abdominal cavity when in an upright position.
Paraesophageal or Rolling Hiatal Hernia
The fundus of the stomach can roll up through the diaphragm forming a pocket along the side of the esophagus.
Clinical Manifestations of Hiatal Hernias
- Heartburns
- Dysphagia
- Severe burning pain when bending over (relieved when patient is in upright position)
Hiatal Hernia Therapy
- Reduce intra-abdominal pressure
- Use of a Antacids and antisecretory agents
- Weight loss management
What should you teach your patient with a hiatal hernia to do to reduce intra-abdominal pressure?
Eat small meals Wear loose clothing Avoid heavy lifting Stop alcohol and tobacco use (gastric irritants) Keep HOB up to sleep
Drugs to treat Hiatal Hernias
H2 receptor blockers: Tagamet, Zantac, Pepsid
PPI’s: Prevacid, Protonix, Nexium
Cholinergics: Bethanechol
Prokinetic-motility enhancing: Reglan
Why are H2 Receptor Blockers and PPI’s used to treat hiatal hernias?
Decreases acidity of stomach
Why are Cholinergic used to treat hiatal hernias?
Use to increase LES pressure and increase gastric emptying
Why are pro kinetic-motility enhancing drugs used to treat hiatal hernias?
Promotes gastric emptying
Diagnostic Findings of Hiatal Hernias
- Barium Swallow
- Endoscopic visualization of lower esophagus
- Upper GI endoscopy
- Motility Studies
Endoscopic visualization of the lower esophagus in patients with a hiatal hernia will show
Mucosal abnormalities of any inflamamtion
What will show on a barium swallow in a patient with hiatal hernia?
Protrusion of gastric mucosa through esophageal hiatus.
Non-Conservative Therapies for Hiatal Hernias
- Surgery
- Reduction of the herniated stomach into abdomen
- Herniotomy
- Herniorraphy
- Gastropexy
Herniotomy
Excision of the hernial sac
Herniorraphy
Closure of the hiatal defect
Gastropexy
Attachment of the stomach subdiaphragmatically to prevent reherniation.
Complications of Hiatal Hernias
GERD Esophagitis Hemorrhage from erosion Stenosis of esophagus Ulcers in herniated part of the stomach Strangulation of the hernia (twisting - limits O2 supply -> increases risk for ulceration) Regurgitation with tracheal aspiration
Gastritis
Inflammation of the gastric mucosa.
Acute or Chronic
Diffuse or localized
Pathophysiology: Gastritis
- A result of the breakdown of the normal gastric mucosa barrier that protects the stomach from corrosive action of HCL acid and pepsin.
- HCL and pepsin diffuse back into the mucosa causing edema, capillary walls to lose plasma into gastric lumen and possible hemorrhage.
How can you treat acute gastritis?
Eliminating the cause is all that is needed to treat acute gastritis.
If vomiting occurs, rest, NPO status and IVF may be prescribed.
In severe cases of acute gastritis, what should be done?
NGT will be used to monitor for bleeding, for lavage of the precipitating agent from the stomach and to keep the stomach empty.
Chronic Gastritis: Management is focused on
Evaluating and then eliminating the specific cause.
Such as drugs, alcohol, h.pylori and pernicious anemia.
How can pernicious anemia lead to chronic gastritis?
Decreased oxygenation to the stomach -> threatens the integrity of mucous membranes -> gastritis
Risk factors for gastritis
- Drug related: NSAIDs
- Diet: alcohol, spicy foods
- H. Pylori infection
- Autoimmune metaplastic atrophic gastritis
What risk factors for NSAID are related to Gastritis?
- Female
- Over age of 60
- History of ulcer disease
- Concomitant use of anticoagulants
- Use of other NSAIDs
- Use of corticosteroids
- Having a chronic debilitating disorder
Autoimmune metaplastic atrophic gastritis
An immune response against parietal cells
Clinical Manifestations of Acute Gastritis
Anorexia
N/V
Epigastric Tenderness
Feeling of Fullness
Clinical Manifestations of Chronic Gastritis
Same as acute gastritis PLUS
Loss of parietal cells -> loss of IF -> decreased absorption of cobalamin -> PERNICIOUS ANEMIA
Diagnostic Findings for patients with Gastritis
- Diagnosis based on pt history of drug and alcohol use
- Endoscopic exams with biopsy for definitive diagnosis
- For H. Pylori: breath serum, stool and urine tests
- Stool for occult blood
- Serum for anemia or lack of IF
- Serum for antibodies to parietal cells and IF
Peptic Ulcer Disease
Condition characterized by erosion of the GI mucosa resulting from digestive action of HCl acid and pepsin.
Types of Peptic Ulcer Disease
- Acute Ulcer - superficial, minimal inflammation
2. Chronic Ulcer - duration is longstanding
Type of Ulcerations
- Gastric Ulceration
- Duodenal Ulcers
- Physiologic Stress Ulcer
Clinical Manifestations of Peptic Ulcer Disease
May have no pain
Burning or cramp like (food can irritate it)
Back Pain
Complications of PUD
Hemorrhage
Perforation
Gastric Outlet Obstruction
Nursing Therapeutics for PUD
- Adequate rest
- Bland diet
- Cessation of smoking
- Aspirin and NSAIDs should be DISCONTINUED
- Drugs
- Nutritional Therapy (6 small meals)
What drugs are used to treat PUD?
- H2R Blockers (decrease HCl acid secretion)
- PPI’s (decrease HCl acid secretion)
- Antibiotics (to treat H. Pylori infection)
- Antacids (as adjuvant therapy - neutralizes gastric acid)
- Anticholinergic Drugs (decrease stimulation of HCl)
- Cytoprotective drugs (increases mucosal protection)
Ulcerative Colitis
- Characterized by inflammation and ulceration of the colon and rectum.
- Colon may become hyperemic or edematous; may develop abscess then ulceration.
Clinical Manifestations of Ulcerative Colitis
Bloody diarrhea (d/t ulceration) Abdominal Pain 4-5 stools/day -> dehydration Fever, malaise, anorexia -> weight loss Anemia (d/t malnutrition) Tachycardia (d/t decreased O2 delivery from anemia)
Goals of Nursing Care for Patients with Ulcerative Colitis
Rest the bowel Control Inflammation Combat infections Alleviate stress Symptomatic relief
Drug Therapy for Ulcerative Colitis
Antimicrobial
Corticosteroid
Sedative
Antidiarrheal
Treatment of Ulcerative Colitis
Surgical Intervention
Drug Therapy
Nutritional Therapy (NPO, high caloric diet, TPN, vitamins)
Surgical Interventions for patients with Ulcerative Colitis
Proctocolectomy with ileostomy: ileostomy vs colostomy
What is the difference between a colostomy and ileostomy?
In ileostomy: the fecal matter is still liquid
In colostomy: the fecal matter is more shaped and formed (water has been absorbed in large intestine)
Crohn’s Disease
Chronic, non-specific inflammatory disease of the bowel.
Cause is unknown.
Can occur anywhere along the GI tract (from mouth to anus).
Characteristics of Crohn’s Disease
Inflammation of segments of the GI tract.
Most often seen in the terminal ileum, jejunum and colon.
Areas involved are usually discontinuous with segments of normal bowel.
Clinical Manifestations of Crohn’s Disease
Diarrhea* Abdominal Pain* Fatigue Weight loss, malnutrition Dehydration Fever
Goals for Treatment of Crohn’s Disease
Control of inflammatory process
Relief of symptoms
Correct nutritional and metabolic problems
Treatment for Crohn’s Disease
Drug Therapy Nutritional Therapy (low residue diet, high caloric diet)
What drugs are used to treat Crohn’s?
Sulfasalazine (decreases infection potential)
Corticosteroid (decreases inflammatory process)
Flagyl (anti-infective)
Diverticulum
Saccular dilation or out pouching of the mucosa through the circular smooth muscle of the intestinal wall.
Common in sigmoid colon.
Diverticulosis
Non inflamed diverticula
Diverticulitis
Inflammation of the diverticula and increased luminal pressures -> erosion of bowel wall -> perforation into peritoneum.
What is the cause of Diverticulitis or Diverticulosis?
Cause is unknown but deficiency in dietary fiber has been associated with its development.
Clinical Manifestations of Diverticulosis or Diverticulitis
- Can be asymptomatic
- Crampy abdominal pain LLQ relieved by flatus of BM
- Alternating constipation and diarrhea
- Fever, chills, n/v, anorexia
- Increase in WBC (if inflammation)
Collaborative Care for Diverticulitis or Diverticulosis
- Uncomplicated diverticula - increase fiber in the diet
- Bulk laxative
- increase fluid intake
- weight reduction (decreases abdominal pressure)
- prevent intra-abdominal pressure
- NPO, bed rest
- No “seeds” in the diet (can lodge into diverticula and create irritation and inflammation)
What can decrease the risk for Crohn’s Disease?
High fiber and fruit
Crohn’s Disease: Pattern of Inflammation
- Involves ALL layers of the bowel wall.
- Strictures -> bowel obstruction.
- Skip lesions
- Ulcerations deep and longitudinal: “cobble stone appearance”
Since inflammation from Crohn’s goes through the entire wall,
microscopic leaks allow bowel content to enter peritoneal cavity -> abscesses or produce peritonitis
Skip lesions
Segments of normal bowel between diseased portion.
Complications of Crohn’s Disease
- Fistulas
- Hemorrhage -> anemia
- Colonic Dilation
- Nutritional Problemss
- Short Bowel Syndrome
Fistulas
Abnormal connection between organs.
Occurs between adjacent areas of bowel; bowel and bladder; bowel and vagina; forms tract through skin to outside body.
UTI’s are the first sign of
A bowel/bladder fistula.
Feces can be seen in urine.
Colonic Dilation
Toxic megacolon
More common in UC
Leads to perforation.
Emergency situation.
What nutritional problems can arise from Crohn’s disease?
Cobalamin and bile salts are absorbed in terminal ileum so if there is disease there -> fat malabsorption and anemia.
Short Bowel Syndrome
- Surgery/Disease leaves little surface area of SI to maintain life -> severe absorption issues.
- Life TPN is necessary: given IV
What can decrease the risk for ulcerative colitis?
Vegetables
Ulcerative Colitis: Pattern of Inflammation
Usually starts in the rectum and moves toward cecum.
Inflammation and ulceration occurs in the MUCOSAL layer (innermost layer).
Complications of Ulcerative Colitis
- Fistulas and abscesses are rare since inflammation doesn’t extend through all bowel wall layers.
- Breakdown of cells -> protein loss in stool
- F&E cannot be absorbed through inflamed mucosa
- Hemorrhage -> anemia
- Colonic Dilation
- Systemic Problems
Colonic dilation Symptoms
Patient has fever, increased ab pain and shock.
S&S of shock: tachycardia, hypotension, dyspnea, decreased SpO2.
System Complications that can be caused by Ulcerative Colitis
Joint, eye, mouth, kidney, bone, vascular and skin problems.
Circulating cytokines trigger inflammation in these areas.
Diagnostic Studies for IBD
- CBC: shows iron deficiency anemia
- Elevated WBC: indicates toxic megacolon or perforation
- Decreased serum Na, K, Cl, Bicarbonate, Mg (d/t F&E lost during vomiting and diarrhea)
- Hypoalbuminemia
- Stool cultures: to determine if infection is present
- Imaging studies
- Colonoscopy
- Capsule endoscopy
Imaging Studies for IBD
- Double-contrast barium enema
- Small bowel series
- Trans abdominal ultrasound
- CT, MRI
Capsule Endoscopy in IBD
AIDS in diagnoses in Crohn’s Disease in SI; colonoscopy can only reach distal ileum.
Step-up Approach
Use less toxic therapies first and move to more toxic.
Includes aminosalicylates and Antimicrobial
Step-down approach
Toxic medications first.
Use biologic and targeted therapy first.
Antidiarrheal medications can be given unless
Patient is having acute exacerbations.
If having acute inflammation with increased diarrhea and given antidiarrheal medication, it will increase risk for colonic dilation.
Aminosalicyclates includes
Sulfasalazine
Comes in the form of suppositories, enemas and foams (topical treatment)
Aminosalicyclates: Sulfasalazine
Minimizes systemic effects -> first line treatment.
Decrease GI inflammation through direct contact w. Bowel mucosa.
Side Effects of Aminosalicyclates (Sulfasalazine)
May cause yellowish orange discoloration of skin/urine
Photosensitivity
Antimicrobials for IBD
Metronidazole
Prevents or treats secondary infection.
Corticosteroids
Includes Prednisone
Decreases inflammation
Given shortest time possible
Secondary Treatment
Patients taking corticosteroids should receive
Ca or K supplements because corticosteroids -> Na retention, loss of K and toxic megacolon
Immunosuppressants
Include methotrexate
Suppress immune response
Used after corticosteroid therapy.
Immunosuppressants require
Require regular CBC monitoring d/t bone marrow suppression.
Cytokines Tumor Necrosis Factor Inhibitor
Prevents migration of leukocytes from blood stream to inflamed tissue.
What should you monitor for patients taking cytokine tumor necrosis factor inhibitors?
Monitor CBC d/t risk for depression of bone marrow and decrease T-cell which leads to anemia.
Pt more at risk for infection on this therapy. Watch for infection.
Why should you quit smoking if you have IBD?
Smoking stimulates GI tract.
Diverticulosis and Diverticulitis is associated with
High luminal pressure from deficiency in dietary fiber intake.
How does fiber intake possible cause diverticulosis and diverticulitis?
Inadequate fiber slows transit time -> water absorbed from stool -> difficult to pass through lumen.
Decreased stool size raises intraluminal pressure.
Complications of Diverticulitis or Diverticulosis
- Perforation and Abscess
- Blockage
- Bleeding
- Peritonitis (CRITICAL and requires surgery)
- Fistula
Add upper GI problems
From mentor study guide
