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NURS 306 > GI Disorders And Drugs Affecting The GI System > Flashcards

GI Disorders And Drugs Affecting The GI System Flashcards

1
Q

Gastroesophageal Reflux Disease (GERD)

A

Reflux of acid and pepsin or bile salts from the stomach to the esophagus.
Lower esophageal sphincter problem.

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2
Q

Gastroesophageal Reflux Disease is also known as

A

Reflux esophagitis

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3
Q

GERD: Inflammation of the esophagus/inflammatory responses include:

A 
Hyperemia
Edema
Increased Capillary Permeability 
Erosion
Ulceration
Increased risk of pre-cancer or pre-neoplastic lesion (Barrett's esophagus)
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4
Q

Risk Factors for GERD

A 
Older Age
Obesity
Hiatal Hernia
Certain Medications
Pregnancy
Lifestyle and dietary habits
Conditions that increase abdominal ?
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5
Q

A normal functioning lower esophageal sphincter maintains

A

A zone of high pressure to prevent Chyme reflux

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6
Q

Clinical Manifestations of GERD

A 
Heartburn
Upper abdominal or mid-epigastric pain within 1 hour of eating
Dysphasia
Chronic Cough (Non-productive)
Metallic Taste, Unpleasant Taste
Nausea
Weight loss
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7
Q

Symptoms of GERD are worse when

A

Lying down

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8
Q

In babies, clinical manifestations of GERD include

A

Vomiting (6-12 months)
Failure to thrive in infants
Impaired growth in children

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9
Q

Diagnostics for GERD

A

Esophageal endoscopy

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10
Q

Treatment for GERD

A 
Drugs such as antacids, histamine 2 receptor antagonists, proton pump inhibitors
Lifestyle changes
Reflux precautions (elevate head of bed, don't exercise after eating, don't lie down after eating) smoking cessation, weight management
May consider fundoplication if traditional not working
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11
Q

Fundoplication

A

The surgical procedure of tucking or folding the fundus of the stomach around the esophagus to prevent reflux, used in the repair of a hiatal hernia.

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12
Q

Peptic Ulcer Disease

A

A break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum

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13
Q

Zollinger-Ellison Syndrome

A

“Gastrinomas” tumor(s) in pancreas or small intestine (duodenum) secrete large amounts of gastric hormone causes increase production of acid

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14
Q

Risk Factors for Peptic Ulcer Disease

A 
Alcohol
Smoking
Age
Stress
Infection (H. Pylori)
Medications (eg. NSAIDs)
Chronic diseases
Type O blood
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15
Q

What are the types of Peptic Ulcers?

A
  1. Duodenal Ulcer
  2. Gastric Ulcer
  3. Stress Ulcer
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16
Q

Duodenal Ulcer

A

Ulcer of the duodenum - Most common type

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17
Q

Major causes of DU

A 
Helicobacter pylori (H. Pylori)
NSAIDs
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18
Q

Clinical Manifestations of Duodenal Ulcers

A

Mid-epigastric pain 2 or 3 hours after eating (when the stomach is empty)

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19
Q

Duodenal Ulcer Pain

A

May occur in the middle of the night
May be relieved quickly by ingesting antacids or food
“Pain-Food-Relief Pattern”

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20
Q

Diagnostics for Dudoenal Uclers

A

Esophageal Endoscopy
Barium Swallow
(For H. Pylori infection: urea breath test, biopsy, H.pylori antibody)

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21
Q

Treatments for Duodenal Ulcers

A

Drugs such as antacids, histamine 2 receptor antagonists, proton pump inhibitors
Surgery if severe
For H. Pylori infection: combination drugs such as Bismuth, Metronidiazole or Clarithromycin, Amoxicillin or Tetracycline

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22
Q

Gastric Ulcer

A

Ulcer of the stomach - Less common than DU

Tends to be chronic and increases risk for gastric cancer

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23
Q

Gastric Ulcers are common in

A

The elderly

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24
Q

Primary defect of Gastric Ulcers is

A

An increased mucosal permeability to H+ ions

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25
Q

Major causes of Gastric Ulcers

A

Decreased mucosal synthesis of prostaglandin
Bile Reflux
H. Pylori infection
NSAIDs

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26
Q

Clinical Manifestations of Gastric Ulcers

A

Pain-antacid-relief pattern
Food-pain-pattern (when food in stomach)
Loss of appetite → anorexia → weight loss
Nausea and/or vomiting

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27
Q

Treatments for Gastric Ulcers

A

Drugs such as antacids, histamine 2 receptor antagonists, proton pump inhibitors

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28
Q

Stress Ulcer

A

Associated with severe illness, trauma or neural injury

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29
Q

Types of Stress Ulcers include

A
  1. Ischemic Ulcers

2. Cushing Ulcers

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30
Q

Ischemic Ulcers

A

Ulcers that develop within hours of trauma, burns, hemorrhage, sepsis.
Causes ischemia of stomach/duodenal mucosa

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31
Q

Cushing Ulcers

A

Ulcers that develop as a result of head/brain injury, brain surgery
Causes decreased mucosal blood flow and increased acid secretion.

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32
Q

Clinical Manifestations of Stress Ulcers

A

bleeding (uncommon, but occurs more readily)
nausea/vomiting
abdominal pain

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33
Q

Treatment for Stress Ulcers

A

Antacids
Histamine 2 Receptor Antagonists
Proton Pump Inhibitors

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34
Q

Antacids include

A

Most antacids are available OTC:
Magnesium containing antacids (I.e Milk of Magnesia)
Aluminum containing antacids (i.e. Basaljiel, Amphojel, Maalox, Mylanta)
Calcium containing antacids (I.e tums, Maalox)
Sodium containing antacids (Alka-Seltzer)

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35
Q

Mechanism of Action: Antacids

A
  • Work primarily by neutralizing gastric acidity.
  • Promote gastric mucosal defensive mechanisms - stimulates secretion of mucus (mucus protects against destructive actions of hydrochloric acid), prostaglandins (prevents histamine from binding to its corresponding parietal cell receptors, which inhibits the production of adenylate cyclase, w/out adenylate cyclase, no cAMP can be formed and no second messenger is available to activate the proton pump) and bicarbonate (helps buffer the acidity of hydrochloric acid) from the cells inside the gastric glands
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36
Q

Indications: Antacids

A

for acute relief of symptoms associated with peptic ulcer, gastritis, gastric hyperacidity and heartburn.

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37
Q

Contraindications: Antacids

A

Allergy to drug
Severe renal failure or electrolyte disturbances (potential toxic accumulation of electrolytes in the antacids themselves)
GI obstruction

38
Q

Adverse Effects of Antacids

A

Magnesium Antacids: Diarrhea
Aluminum Antacids: Constipation
Calcium Antacids: Constipation, Kidney stones, Rebound hyperacidity. Chronic use of high doses - milk-alkali syndrome.
Excessive use: Systemic Alkalosis

39
Q

Interactions of Antacids

A
  1. Absorption: of other drugs to antacids, which reduces ability of other drug to be absorbed into the body.
  2. Chelation: which is the chemical inactivation of other drugs that produces insoluble complexes
  3. Increased Stomach pH: which increases the absorption of basic drugs and decreases absorption of acidic drugs
  4. Increased Urinary pH: increases the excretion of acidic drugs and decreases the excretion of basic drugs.
40
Q

Nursing Process: Antacids

A
  • caution use in patients who have heart failure, hypertension or other cardiac diseases or require sodium restriction, especially if antacid is high in sodium
  • other meds should be avoided 1-2 hours of taking an antacid
  • needs to be given with at least 8 oz of water to enhance absorption of antacid
41
Q

Proton Pump Inhibitors include

A 
"Prazole"
Lansoprazole 
Omeprazole
Pantoprazole
Rabeprazole 
Esomeprazole
42
Q

Mechanism of Action: Proton Pump Inhibitors

A

block the final step in the acid production pathway
bind irreversibly to the proton pump -> prevents movement of hydrogen ions out of the parietal cell into the stomach and thereby blocks all gastric acid secretion

43
Q

Indications for Proton Pump Inhibitors

A

First line therapy for:
-erosive esophagitis
-symptomatic GERD that is poorly responsive to other medical treatment
-short-term treatment of active duodenal ulcers and active benign gastric ulcers
-gastric hypersecretory conditions
-NSAID-induced ulcers
-stress ulcer prophylaxis.
Can be used in combination w/ antibiotics to treat patients w/ H. pylori infections.

44
Q

Contraindications: Proton Pump Inhibitors

A

known drug allergies

45
Q

Adverse Effects of Proton Pump Inhibitors

A

Usually well tolerated.
Concerns that these drugs may be overprescribed and may predispose patients to GI tract infections (d/t reduction of normal acid-mediated antimicrobial protection)
New concerns that long-term use will lead to development of osteoporosis, risk for C-diff infections, risk for wrist, hip and spine fractures; and pneumonia.

46
Q

Interactions of Proton Pump Inhibitors

A

May increase levels of diazepam and phenytoin.
Increased chance of bleeding in patients who are taking both PPI and warfarin.
Interference w/ absorption of ketoconazole, ampicillin, iron salts and digoxin.
Sucralfate may delay absorption of PPI’s.
Food may decrease absorption of PPI’s.

47
Q

Nursing Process: Proton Pump Inhibitors

A

Recommended that they be taken on an empty stomach.

Assess swallowing ability d/t size of capsules

48
Q

H2-Receptor Antagonists include

A 
"Tidine"
Cimetidine
Famotidine
Ranitidine
Nizatidine
49
Q

Mechanism of Action: H2-Receptor Antagonists

A
  • Competitively block the H2 receptor of acid-producing parietal cells -> parietal cell less responsive not only to histamine but also stimulation of ACh and gastrin.
  • Decreases H+ secretion from parietal cells -> increase in pH of the stomach -> relief of many symptoms associated w/ hyperacidity-related conditions
50
Q

Indications for H2-Receptor Antagonists

A

Treatment of GERD, peptic ulcer disease, and erosive esophagitis.
Adjunct therapy in the control of upper GI tract bleeding and treatment of pathologic gastric hypersecretory conditions.
Commonly used for stress ulcer prophylaxis in critically ill patients.

51
Q

Adverse Effects of H2-Receptor Antagonists

A

Cardiovascular: Hypotension
CNS: Headache, lethargy, confusion, depression, hallucinations, slurred speech, agitation
Endocrine: Increased prolactin secretion, gynecomastia (w/ cimetidine)*
Gastrointestinal: Diarrhea, nausea, abdominal cramps
Genitourinary: Impotence, increased BUN, increased creatinine levels
Hepatobiliary: elevated liver enzyme levels, jaundice
Hematologic: agranulocytosis, thrombocytopenia*, neutropenia, aplastic anemia
Integumentary: urticaria, rash, alopecia, sweating, flushing, exfoliative dermatitis

52
Q

Interactions of H2-Receptor antagonists

A

Cimetidine carries higher risk for drug interactions than the other three drugs. May raise blood concentrations of certain drugs.
Significant interactions are more likely to arise w/ meds having a narrow therapeutic range such as warfarin, lidocaine, phenytoin, theophylline.
All H2 receptor antagonists may inhibit the absorption of certain drugs that require an acidic GI environment for gastric absorption.
Smoking decreases effectiveness of H2 antagonists.

53
Q

Nursing Process: H2-Receptor Antagonists

A

For optimal results, needs to be taken 1-2 hours before antacids.
Assess renal and liver function as well as LOC because of possible drug-related adverse effects.
Do not administer cimetidine and famotidine simultaneously with antacids.

54
Q

Diverticular Disease

A

Presence of saclike outpouching (herniations) of mucosa through muscle layers of colon wall (especially sigmoid)

55
Q

Risk Factors for Diverticular Disease

A

Low-residue/low fiber diet, increasing age

56
Q

Diverticulosis

A

Asymptomatic Diverticular disease

57
Q

Diverticulitis

A

The inflammatory stage of diverticulosis, can lead to: complications such as abscess, rupture, intestinal obstruction and/or peritonitis

58
Q

Clinical Manifestations of Diverticulitis

A 
LLQ abdominal pain
Fever
Nausea
Leukocytosis
Diarrhea or constipation may also occur
May have + hemoccult
59
Q

Treatment for Diverticulitis

A

Antibiotics (for diverticulitis) and/or surgery

60
Q

Prevention of Diverticulitis

A

Increased fiber in diet

Avoid seeds and nuts

61
Q

Ulcerative Colitis

A

Chronic inflammatory disease -> ulceration of the colonic mucosa (rectum and sigmoid colon)

62
Q

Etiology and Pathogenesis of Ulcerative Colitis

A

Genetics, infectious, dietary, immune reactions to intestinal flora (anticolon antibodies)
Colitis (+ mucosal ulceration, esp. in sigmoid colon and rectum)

63
Q

Clinical Manifestations of Ulcerative Colitis

A 
Bloody stools (common), frequent watery diarrhea (10-20 L/day), cramping pain
Periods of remission and exacerbation
64
Q

Ulcerative Colitis increases the risk for

A

Colon cancer

65
Q

Diagnostics for Ulcerative Colitis

A

Sigmoidoscopy
Barium enema
CBC
Stool culture

66
Q

Treatment for Ulcerative Colitis

A

Drugs to treat infection, steroids, immunosuppresive drugs, replacement of fluids and electrolytes , hyperalimentation for severe malnutrition, surgery

67
Q

Crohn’s Disease

A

Granulomatous colitis, oleo colitis or regional enteritis that affects both large and mall intestines (mouth to anus)

68
Q

Etiology and Pathogenesis of Crohn’s Disease

A

+ Inflammation in colon with “skip lesions”
Cobblestone projections of inflamed tissue causing to fistulae
Fissures that extend into lymphatics

69
Q

Risk factors for Crohn’s Disease

A

Similar risk factors and theories of causation as Ulcerative Colitis
Genetic and immunologic factors, smoking, diet, bacteria

70
Q

Clinical Manifestations of Crohn’s Disease

A 
Diarrhea (with mucus), rarely bloody depending on the affected site
Lower abdominal pain/cramping
Weight loss 
Electrolyte and vitamin deficiencies
Anemia (due to malabsorption of Vitamin B12 and folic acid)
Bowel obstruction
Periods of remission and exacerbation
Increased risk of colon cancer
71
Q

Diagnostics for Crohn’s Disease

A

Colonoscopy
Barium Enema
CBC
Stool Culture

72
Q

Treatment for Crohn’s Disease

A

Similar to ulcerative colitis

Surgery to manage fistula, abscess, obstruction and perforation

73
Q

Drugs used to treat Inflammatory Bowel Disease

A

Immunosuppressants and other miscellaneous drugs

74
Q

Intestinal Obstruction

A

Any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion

75
Q

Paralytic ileum

A

Obstruction of the intestines

76
Q

Classifications of Intestinal Obstruction

A

Mechanical and Functional (failure of motility)
Acute and Chronic (or partial)
Location (small or large bowel)

77
Q

Pathogenesis of Intestinal Obstructions

A

Obstruction leads to intestinal distention
Vomiting which causes dehydration and electrolyte disturbances
Can lead to metabolic acidosis
Severe pressure causes ischemia -> necrosis -> perforation -> peritonitis -> SEPSIS

78
Q

Clinical Manifestations of Intestinal Obstruction

A 
Colicky/severe abdominal pain
Pain is constant (acute) 
Nausea and/or vomiting
Abdominal distention and/or tenderness
No bowel sounds
79
Q

Diagnostics for Intestinal Obstructions

A

Ultrasound

Abdominal x-Ray

80
Q

Treatment for Intestinal Obstructions

A

Nasogastric tube (to decompress intestinal lumen to decrease pressure)
Replacement of Fluid and Electrolytes
Surgery

81
Q

Irritable Bowel Syndrome (IBS)

A

“Spastic” colon, irritable colon syndrome

82
Q

The exact etiology and Pathogenesis of IBS is

A

Unclear

83
Q

IBS: GI pathology

A

Absence of GI pathology

84
Q

IBS has

A

Nerve inner actions from brain to gut that affects normal contractions of bowel as it digests and processes food is altered!

85
Q

Theories for IBS

A

Myoelectrical activity of colon is altered resulting in abnormal contractions of colon and intestines or spastic bowel
Previous infection
Genetic factors
Food intolerances: food allergies, or sensitivity
Phsychological: emotional factors associated w/ anxiety, depression and chronic fatigue syndrome
High stress and anxiety levels

86
Q

Clinical Manifestations of IBS

A

alternating pattern of diarrhea, constipation
abdominal discomfort described as cramping or pain
Bloating
Feeling of “obstructed colon”
nausea

87
Q

IBS treatment includes

A

Fiber Supplements: Psyllium (Metamucil) or methylcellulose (Citrucel)
Antidiarrheals
Laxatives
Other meds

88
Q

Selection of drugs for IBS treatment is

A

Symptom directed

89
Q

Antidiarrheal for IBS treatment includes

A

Adsorbents- aluminum hydroxide, bismuth subsalicylate (i.e. Peptobismol)
Anticholinergics- atropine
Opiates- loperamide (i.e. Lomotil)
Probiotics and intestinal flora modifiers- Lactobacillus acidophilus

90
Q

Laxatives for IBS treatments include

A

Bulk-forming – psyllium, methylcellulose
Emollient – docusate, mineral oil
Hyperosmotic – lactulose, magnesium citrate
Stimulant – bisacodyl

91
Q

Sucralfate

A

used for treatment of peptic ulcer disease and stress related ulcers.
binds to tissue proteins in the eroded area and prevents exposure of the ulcerated area to stomach acid

92
Q

Achlorhydria

A

without acid

NURS 306 (26 decks)

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