GI Disorders And Drugs Affecting The GI System Flashcards
Gastroesophageal Reflux Disease (GERD)
Reflux of acid and pepsin or bile salts from the stomach to the esophagus.
Lower esophageal sphincter problem.
Gastroesophageal Reflux Disease is also known as
Reflux esophagitis
GERD: Inflammation of the esophagus/inflammatory responses include:
Hyperemia Edema Increased Capillary Permeability Erosion Ulceration Increased risk of pre-cancer or pre-neoplastic lesion (Barrett's esophagus)
Risk Factors for GERD
Older Age Obesity Hiatal Hernia Certain Medications Pregnancy Lifestyle and dietary habits Conditions that increase abdominal ?
A normal functioning lower esophageal sphincter maintains
A zone of high pressure to prevent Chyme reflux
Clinical Manifestations of GERD
Heartburn Upper abdominal or mid-epigastric pain within 1 hour of eating Dysphasia Chronic Cough (Non-productive) Metallic Taste, Unpleasant Taste Nausea Weight loss
Symptoms of GERD are worse when
Lying down
In babies, clinical manifestations of GERD include
Vomiting (6-12 months)
Failure to thrive in infants
Impaired growth in children
Diagnostics for GERD
Esophageal endoscopy
Treatment for GERD
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
Fundoplication
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.
Peptic Ulcer Disease
A break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum
Zollinger-Ellison Syndrome
“Gastrinomas” tumor(s) in pancreas or small intestine (duodenum) secrete large amounts of gastric hormone causes increase production of acid
Risk Factors for Peptic Ulcer Disease
Alcohol Smoking Age Stress Infection (H. Pylori) Medications (eg. NSAIDs) Chronic diseases Type O blood
What are the types of Peptic Ulcers?
- Duodenal Ulcer
- Gastric Ulcer
- Stress Ulcer
Duodenal Ulcer
Ulcer of the duodenum - Most common type
Major causes of DU
Helicobacter pylori (H. Pylori) NSAIDs
Clinical Manifestations of Duodenal Ulcers
Mid-epigastric pain 2 or 3 hours after eating (when the stomach is empty)
Duodenal Ulcer Pain
May occur in the middle of the night
May be relieved quickly by ingesting antacids or food
“Pain-Food-Relief Pattern”
Diagnostics for Dudoenal Uclers
Esophageal Endoscopy
Barium Swallow
(For H. Pylori infection: urea breath test, biopsy, H.pylori antibody)
Treatments for Duodenal Ulcers
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
Gastric Ulcer
Ulcer of the stomach - Less common than DU
Tends to be chronic and increases risk for gastric cancer
Gastric Ulcers are common in
The elderly
Primary defect of Gastric Ulcers is
An increased mucosal permeability to H+ ions
Major causes of Gastric Ulcers
Decreased mucosal synthesis of prostaglandin
Bile Reflux
H. Pylori infection
NSAIDs
Clinical Manifestations of Gastric Ulcers
Pain-antacid-relief pattern
Food-pain-pattern (when food in stomach)
Loss of appetite → anorexia → weight loss
Nausea and/or vomiting
Treatments for Gastric Ulcers
Drugs such as antacids, histamine 2 receptor antagonists, proton pump inhibitors
Stress Ulcer
Associated with severe illness, trauma or neural injury
Types of Stress Ulcers include
- Ischemic Ulcers
2. Cushing Ulcers
Ischemic Ulcers
Ulcers that develop within hours of trauma, burns, hemorrhage, sepsis.
Causes ischemia of stomach/duodenal mucosa
Cushing Ulcers
Ulcers that develop as a result of head/brain injury, brain surgery
Causes decreased mucosal blood flow and increased acid secretion.
Clinical Manifestations of Stress Ulcers
bleeding (uncommon, but occurs more readily)
nausea/vomiting
abdominal pain
Treatment for Stress Ulcers
Antacids
Histamine 2 Receptor Antagonists
Proton Pump Inhibitors
Antacids include
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)
Mechanism of Action: Antacids
- 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
Indications: Antacids
for acute relief of symptoms associated with peptic ulcer, gastritis, gastric hyperacidity and heartburn.
Contraindications: Antacids
Allergy to drug
Severe renal failure or electrolyte disturbances (potential toxic accumulation of electrolytes in the antacids themselves)
GI obstruction
Adverse Effects of Antacids
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
Interactions of Antacids
- Absorption: of other drugs to antacids, which reduces ability of other drug to be absorbed into the body.
- Chelation: which is the chemical inactivation of other drugs that produces insoluble complexes
- Increased Stomach pH: which increases the absorption of basic drugs and decreases absorption of acidic drugs
- Increased Urinary pH: increases the excretion of acidic drugs and decreases the excretion of basic drugs.
Nursing Process: Antacids
- 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
Proton Pump Inhibitors include
"Prazole" Lansoprazole Omeprazole Pantoprazole Rabeprazole Esomeprazole
Mechanism of Action: Proton Pump Inhibitors
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
Indications for Proton Pump Inhibitors
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.
Contraindications: Proton Pump Inhibitors
known drug allergies
Adverse Effects of Proton Pump Inhibitors
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.
Interactions of Proton Pump Inhibitors
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.
Nursing Process: Proton Pump Inhibitors
Recommended that they be taken on an empty stomach.
Assess swallowing ability d/t size of capsules
H2-Receptor Antagonists include
"Tidine" Cimetidine Famotidine Ranitidine Nizatidine
Mechanism of Action: H2-Receptor Antagonists
- 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
Indications for H2-Receptor Antagonists
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.
Adverse Effects of H2-Receptor Antagonists
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
Interactions of H2-Receptor antagonists
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.
Nursing Process: H2-Receptor Antagonists
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.
Diverticular Disease
Presence of saclike outpouching (herniations) of mucosa through muscle layers of colon wall (especially sigmoid)
Risk Factors for Diverticular Disease
Low-residue/low fiber diet, increasing age
Diverticulosis
Asymptomatic Diverticular disease
Diverticulitis
The inflammatory stage of diverticulosis, can lead to: complications such as abscess, rupture, intestinal obstruction and/or peritonitis
Clinical Manifestations of Diverticulitis
LLQ abdominal pain Fever Nausea Leukocytosis Diarrhea or constipation may also occur May have + hemoccult
Treatment for Diverticulitis
Antibiotics (for diverticulitis) and/or surgery
Prevention of Diverticulitis
Increased fiber in diet
Avoid seeds and nuts
Ulcerative Colitis
Chronic inflammatory disease -> ulceration of the colonic mucosa (rectum and sigmoid colon)
Etiology and Pathogenesis of Ulcerative Colitis
Genetics, infectious, dietary, immune reactions to intestinal flora (anticolon antibodies)
Colitis (+ mucosal ulceration, esp. in sigmoid colon and rectum)
Clinical Manifestations of Ulcerative Colitis
Bloody stools (common), frequent watery diarrhea (10-20 L/day), cramping pain Periods of remission and exacerbation
Ulcerative Colitis increases the risk for
Colon cancer
Diagnostics for Ulcerative Colitis
Sigmoidoscopy
Barium enema
CBC
Stool culture
Treatment for Ulcerative Colitis
Drugs to treat infection, steroids, immunosuppresive drugs, replacement of fluids and electrolytes , hyperalimentation for severe malnutrition, surgery
Crohn’s Disease
Granulomatous colitis, oleo colitis or regional enteritis that affects both large and mall intestines (mouth to anus)
Etiology and Pathogenesis of Crohn’s Disease
+ Inflammation in colon with “skip lesions”
Cobblestone projections of inflamed tissue causing to fistulae
Fissures that extend into lymphatics
Risk factors for Crohn’s Disease
Similar risk factors and theories of causation as Ulcerative Colitis
Genetic and immunologic factors, smoking, diet, bacteria
Clinical Manifestations of Crohn’s Disease
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
Diagnostics for Crohn’s Disease
Colonoscopy
Barium Enema
CBC
Stool Culture
Treatment for Crohn’s Disease
Similar to ulcerative colitis
Surgery to manage fistula, abscess, obstruction and perforation
Drugs used to treat Inflammatory Bowel Disease
Immunosuppressants and other miscellaneous drugs
Intestinal Obstruction
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
Paralytic ileum
Obstruction of the intestines
Classifications of Intestinal Obstruction
Mechanical and Functional (failure of motility)
Acute and Chronic (or partial)
Location (small or large bowel)
Pathogenesis of Intestinal Obstructions
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
Clinical Manifestations of Intestinal Obstruction
Colicky/severe abdominal pain Pain is constant (acute) Nausea and/or vomiting Abdominal distention and/or tenderness No bowel sounds
Diagnostics for Intestinal Obstructions
Ultrasound
Abdominal x-Ray
Treatment for Intestinal Obstructions
Nasogastric tube (to decompress intestinal lumen to decrease pressure)
Replacement of Fluid and Electrolytes
Surgery
Irritable Bowel Syndrome (IBS)
“Spastic” colon, irritable colon syndrome
The exact etiology and Pathogenesis of IBS is
Unclear
IBS: GI pathology
Absence of GI pathology
IBS has
Nerve inner actions from brain to gut that affects normal contractions of bowel as it digests and processes food is altered!
Theories for IBS
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
Clinical Manifestations of IBS
alternating pattern of diarrhea, constipation
abdominal discomfort described as cramping or pain
Bloating
Feeling of “obstructed colon”
nausea
IBS treatment includes
Fiber Supplements: Psyllium (Metamucil) or methylcellulose (Citrucel)
Antidiarrheals
Laxatives
Other meds
Selection of drugs for IBS treatment is
Symptom directed
Antidiarrheal for IBS treatment includes
Adsorbents- aluminum hydroxide, bismuth subsalicylate (i.e. Peptobismol)
Anticholinergics- atropine
Opiates- loperamide (i.e. Lomotil)
Probiotics and intestinal flora modifiers- Lactobacillus acidophilus
Laxatives for IBS treatments include
Bulk-forming – psyllium, methylcellulose
Emollient – docusate, mineral oil
Hyperosmotic – lactulose, magnesium citrate
Stimulant – bisacodyl
Sucralfate
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
Achlorhydria
without acid
