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NURS 313R > Exam 2: GI Disorders > Flashcards

Exam 2: GI Disorders Flashcards

1
Q

Hiatal Hernia

A

Protrusion of a portion of the stomach into the esophagus through an opening or hiatus in the diaphragm.

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2
Q

Types of Hiatal Hernia

A
  1. Sliding Hiatal Hernia

2. Paraesophageal or rolling Hiatal Hernia

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3
Q

Sliding Hiatal Hernia

A

When the stomach slides into the thoracic cavity when in supine position and slides back into the abdominal cavity when in an upright position.

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4
Q

Paraesophageal or Rolling Hiatal Hernia

A

The fundus of the stomach can roll up through the diaphragm forming a pocket along the side of the esophagus.

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5
Q

Clinical Manifestations of Hiatal Hernias

A
  • Heartburns
  • Dysphagia
  • Severe burning pain when bending over (relieved when patient is in upright position)
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6
Q

Hiatal Hernia Therapy

A
  • Reduce intra-abdominal pressure
  • Use of a Antacids and antisecretory agents
  • Weight loss management
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7
Q

What should you teach your patient with a hiatal hernia to do to reduce intra-abdominal pressure?

A 
Eat small meals
Wear loose clothing
Avoid heavy lifting
Stop alcohol and tobacco use (gastric irritants)
Keep HOB up to sleep
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8
Q

Drugs to treat Hiatal Hernias

A

H2 receptor blockers: Tagamet, Zantac, Pepsid
PPI’s: Prevacid, Protonix, Nexium
Cholinergics: Bethanechol
Prokinetic-motility enhancing: Reglan

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9
Q

Why are H2 Receptor Blockers and PPI’s used to treat hiatal hernias?

A

Decreases acidity of stomach

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10
Q

Why are Cholinergic used to treat hiatal hernias?

A

Use to increase LES pressure and increase gastric emptying

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11
Q

Why are pro kinetic-motility enhancing drugs used to treat hiatal hernias?

A

Promotes gastric emptying

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12
Q

Diagnostic Findings of Hiatal Hernias

A
  • Barium Swallow
  • Endoscopic visualization of lower esophagus
  • Upper GI endoscopy
  • Motility Studies
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13
Q

Endoscopic visualization of the lower esophagus in patients with a hiatal hernia will show

A

Mucosal abnormalities of any inflamamtion

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14
Q

What will show on a barium swallow in a patient with hiatal hernia?

A

Protrusion of gastric mucosa through esophageal hiatus.

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15
Q

Non-Conservative Therapies for Hiatal Hernias

A
  • Surgery
  • Reduction of the herniated stomach into abdomen
  • Herniotomy
  • Herniorraphy
  • Gastropexy
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16
Q

Herniotomy

A

Excision of the hernial sac

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17
Q

Herniorraphy

A

Closure of the hiatal defect

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18
Q

Gastropexy

A

Attachment of the stomach subdiaphragmatically to prevent reherniation.

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19
Q

Complications of Hiatal Hernias

A 
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
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20
Q

Gastritis

A

Inflammation of the gastric mucosa.
Acute or Chronic
Diffuse or localized

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21
Q

Pathophysiology: Gastritis

A
  • 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.
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22
Q

How can you treat acute gastritis?

A

Eliminating the cause is all that is needed to treat acute gastritis.
If vomiting occurs, rest, NPO status and IVF may be prescribed.

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23
Q

In severe cases of acute gastritis, what should be done?

A

NGT will be used to monitor for bleeding, for lavage of the precipitating agent from the stomach and to keep the stomach empty.

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24
Q

Chronic Gastritis: Management is focused on

A

Evaluating and then eliminating the specific cause.

Such as drugs, alcohol, h.pylori and pernicious anemia.

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25
Q

How can pernicious anemia lead to chronic gastritis?

A

Decreased oxygenation to the stomach -> threatens the integrity of mucous membranes -> gastritis

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26
Q

Risk factors for gastritis

A
  • Drug related: NSAIDs
  • Diet: alcohol, spicy foods
  • H. Pylori infection
  • Autoimmune metaplastic atrophic gastritis
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27
Q

What risk factors for NSAID are related to Gastritis?

A
  • 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
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28
Q

Autoimmune metaplastic atrophic gastritis

A

An immune response against parietal cells

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29
Q

Clinical Manifestations of Acute Gastritis

A

Anorexia
N/V
Epigastric Tenderness
Feeling of Fullness

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30
Q

Clinical Manifestations of Chronic Gastritis

A

Same as acute gastritis PLUS

Loss of parietal cells -> loss of IF -> decreased absorption of cobalamin -> PERNICIOUS ANEMIA

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31
Q

Diagnostic Findings for patients with Gastritis

A
  • 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
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32
Q

Peptic Ulcer Disease

A

Condition characterized by erosion of the GI mucosa resulting from digestive action of HCl acid and pepsin.

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33
Q

Types of Peptic Ulcer Disease

A
  1. Acute Ulcer - superficial, minimal inflammation

2. Chronic Ulcer - duration is longstanding

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34
Q

Type of Ulcerations

A
  1. Gastric Ulceration
  2. Duodenal Ulcers
  3. Physiologic Stress Ulcer
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35
Q

Clinical Manifestations of Peptic Ulcer Disease

A

May have no pain
Burning or cramp like (food can irritate it)
Back Pain

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36
Q

Complications of PUD

A

Hemorrhage
Perforation
Gastric Outlet Obstruction

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37
Q

Nursing Therapeutics for PUD

A
  • Adequate rest
  • Bland diet
  • Cessation of smoking
  • Aspirin and NSAIDs should be DISCONTINUED
  • Drugs
  • Nutritional Therapy (6 small meals)
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38
Q

What drugs are used to treat PUD?

A
  • 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)
39
Q

Ulcerative Colitis

A
  • Characterized by inflammation and ulceration of the colon and rectum.
  • Colon may become hyperemic or edematous; may develop abscess then ulceration.
40
Q

Clinical Manifestations of Ulcerative Colitis

A 
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)
41
Q

Goals of Nursing Care for Patients with Ulcerative Colitis

A 
Rest the bowel
Control Inflammation
Combat infections
Alleviate stress
Symptomatic relief
42
Q

Drug Therapy for Ulcerative Colitis

A

Antimicrobial
Corticosteroid
Sedative
Antidiarrheal

43
Q

Treatment of Ulcerative Colitis

A

Surgical Intervention
Drug Therapy
Nutritional Therapy (NPO, high caloric diet, TPN, vitamins)

44
Q

Surgical Interventions for patients with Ulcerative Colitis

A

Proctocolectomy with ileostomy: ileostomy vs colostomy

45
Q

What is the difference between a colostomy and ileostomy?

A

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)

46
Q

Crohn’s Disease

A

Chronic, non-specific inflammatory disease of the bowel.
Cause is unknown.
Can occur anywhere along the GI tract (from mouth to anus).

47
Q

Characteristics of Crohn’s Disease

A

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.

48
Q

Clinical Manifestations of Crohn’s Disease

A 
Diarrhea*
Abdominal Pain*
Fatigue
Weight loss, malnutrition
Dehydration
Fever
49
Q

Goals for Treatment of Crohn’s Disease

A

Control of inflammatory process
Relief of symptoms
Correct nutritional and metabolic problems

50
Q

Treatment for Crohn’s Disease

A 
Drug Therapy
Nutritional Therapy (low residue diet, high caloric diet)
51
Q

What drugs are used to treat Crohn’s?

A

Sulfasalazine (decreases infection potential)
Corticosteroid (decreases inflammatory process)
Flagyl (anti-infective)

52
Q

Diverticulum

A

Saccular dilation or out pouching of the mucosa through the circular smooth muscle of the intestinal wall.
Common in sigmoid colon.

53
Q

Diverticulosis

A

Non inflamed diverticula

54
Q

Diverticulitis

A

Inflammation of the diverticula and increased luminal pressures -> erosion of bowel wall -> perforation into peritoneum.

55
Q

What is the cause of Diverticulitis or Diverticulosis?

A

Cause is unknown but deficiency in dietary fiber has been associated with its development.

56
Q

Clinical Manifestations of Diverticulosis or Diverticulitis

A
  • 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)
57
Q

Collaborative Care for Diverticulitis or Diverticulosis

A
  • 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)
58
Q

What can decrease the risk for Crohn’s Disease?

A

High fiber and fruit

59
Q

Crohn’s Disease: Pattern of Inflammation

A
  • Involves ALL layers of the bowel wall.
  • Strictures -> bowel obstruction.
  • Skip lesions
  • Ulcerations deep and longitudinal: “cobble stone appearance”
60
Q

Since inflammation from Crohn’s goes through the entire wall,

A

microscopic leaks allow bowel content to enter peritoneal cavity -> abscesses or produce peritonitis

61
Q

Skip lesions

A

Segments of normal bowel between diseased portion.

62
Q

Complications of Crohn’s Disease

A
  • Fistulas
  • Hemorrhage -> anemia
  • Colonic Dilation
  • Nutritional Problemss
  • Short Bowel Syndrome
63
Q

Fistulas

A

Abnormal connection between organs.

Occurs between adjacent areas of bowel; bowel and bladder; bowel and vagina; forms tract through skin to outside body.

64
Q

UTI’s are the first sign of

A

A bowel/bladder fistula.

Feces can be seen in urine.

65
Q

Colonic Dilation

A

Toxic megacolon
More common in UC
Leads to perforation.
Emergency situation.

66
Q

What nutritional problems can arise from Crohn’s disease?

A

Cobalamin and bile salts are absorbed in terminal ileum so if there is disease there -> fat malabsorption and anemia.

67
Q

Short Bowel Syndrome

A
  • Surgery/Disease leaves little surface area of SI to maintain life -> severe absorption issues.
  • Life TPN is necessary: given IV
68
Q

What can decrease the risk for ulcerative colitis?

A

Vegetables

69
Q

Ulcerative Colitis: Pattern of Inflammation

A

Usually starts in the rectum and moves toward cecum.

Inflammation and ulceration occurs in the MUCOSAL layer (innermost layer).

70
Q

Complications of Ulcerative Colitis

A
  • 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
71
Q

Colonic dilation Symptoms

A

Patient has fever, increased ab pain and shock.

S&S of shock: tachycardia, hypotension, dyspnea, decreased SpO2.

72
Q

System Complications that can be caused by Ulcerative Colitis

A

Joint, eye, mouth, kidney, bone, vascular and skin problems.

Circulating cytokines trigger inflammation in these areas.

73
Q

Diagnostic Studies for IBD

A
  • 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
74
Q

Imaging Studies for IBD

A
  • Double-contrast barium enema
  • Small bowel series
  • Trans abdominal ultrasound
  • CT, MRI
75
Q

Capsule Endoscopy in IBD

A

AIDS in diagnoses in Crohn’s Disease in SI; colonoscopy can only reach distal ileum.

76
Q

Step-up Approach

A

Use less toxic therapies first and move to more toxic.

Includes aminosalicylates and Antimicrobial

77
Q

Step-down approach

A

Toxic medications first.

Use biologic and targeted therapy first.

78
Q

Antidiarrheal medications can be given unless

A

Patient is having acute exacerbations.
If having acute inflammation with increased diarrhea and given antidiarrheal medication, it will increase risk for colonic dilation.

79
Q

Aminosalicyclates includes

A

Sulfasalazine

Comes in the form of suppositories, enemas and foams (topical treatment)

80
Q

Aminosalicyclates: Sulfasalazine

A

Minimizes systemic effects -> first line treatment.

Decrease GI inflammation through direct contact w. Bowel mucosa.

81
Q

Side Effects of Aminosalicyclates (Sulfasalazine)

A

May cause yellowish orange discoloration of skin/urine

Photosensitivity

82
Q

Antimicrobials for IBD

A

Metronidazole

Prevents or treats secondary infection.

83
Q

Corticosteroids

A

Includes Prednisone
Decreases inflammation
Given shortest time possible
Secondary Treatment

84
Q

Patients taking corticosteroids should receive

A

Ca or K supplements because corticosteroids -> Na retention, loss of K and toxic megacolon

85
Q

Immunosuppressants

A

Include methotrexate
Suppress immune response
Used after corticosteroid therapy.

86
Q

Immunosuppressants require

A

Require regular CBC monitoring d/t bone marrow suppression.

87
Q

Cytokines Tumor Necrosis Factor Inhibitor

A

Prevents migration of leukocytes from blood stream to inflamed tissue.

88
Q

What should you monitor for patients taking cytokine tumor necrosis factor inhibitors?

A

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.

89
Q

Why should you quit smoking if you have IBD?

A

Smoking stimulates GI tract.

90
Q

Diverticulosis and Diverticulitis is associated with

A

High luminal pressure from deficiency in dietary fiber intake.

91
Q

How does fiber intake possible cause diverticulosis and diverticulitis?

A

Inadequate fiber slows transit time -> water absorbed from stool -> difficult to pass through lumen.
Decreased stool size raises intraluminal pressure.

92
Q

Complications of Diverticulitis or Diverticulosis

A
  • Perforation and Abscess
  • Blockage
  • Bleeding
  • Peritonitis (CRITICAL and requires surgery)
  • Fistula
93
Q

Add upper GI problems

A

From mentor study guide

NURS 313R (18 decks)

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