Drugs for Gastrointestinal Problemsp

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Flashcards covering drugs for gastrointestinal problems including acid-controlling drugs, diarrhea treatments, constipation treatments, and antiemetic/antinausea drugs.

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134 Terms

1
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What are the main functions of the digestive system?

Performs mechanical and chemical digestion, absorbs nutrients, and eliminates waste.

2
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What structures compose the digestive system?

Mouth, esophagus, stomach, intestines, and accessory structures.

3
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What digestive variables are commonly found in very young and older adult patients?

Changes in GI blood flow, amount of surface available, and motility.

4
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What substances does the stomach secrete?

Hydrochloric acid (HCl), Bicarbonate, Pepsinogen, Intrinsic factor, Mucus, and Prostaglandins.

5
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What is the primary function of parietal cells in the gastric gland?

Produce and secrete HCl.

6
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What substances stimulate the secretion of hydrochloric acid?

Food, caffeine, chocolate, alcohol, large fatty meals, and emotional stress.

7
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What is the typical pH range maintained by HCl in the stomach?

pH of 1 to 4.

8
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What do chief cells secrete and what is its function?

They secrete pepsinogen, a proenzyme that becomes pepsin when activated by acid, which then breaks down proteins.

9
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What is the function of mucous cells in the stomach?

They secrete mucus to provide a protective coat against self-digestion by HCl and digestive enzymes.

10
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What is Peptic Ulcer Disease (PUD)?

Gastric or duodenal ulcers that involve digestion of the GI mucosa by the enzyme pepsin.

11
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What bacterium is commonly associated with peptic ulcer disease?

Helicobacter pylori (H. pylori).

12
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What is the first-line therapy for H. pylori-induced ulcers?

A 10- to 14-day course of a proton pump inhibitor (PPI) and clarithromycin plus either amoxicillin or metronidazole, or a combination of a PPI, bismuth subsalicylate, tetracycline, and metronidazole.

13
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What factors predispose ICU patients to GI bleeding from stress-related mucosal damage?

Decreased blood flow, mucosal ischemia, hypoperfusion, reperfusion injury, nasogastric (NG) tubes, and ventilators.

14
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What drugs are given to prevent stress ulcers in ICU patients?

A histamine receptor-blocking drug or a PPI.

15
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What are the main types of acid-controlling drugs?

Antacids, H2 antagonists, and PPIs.

16
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What are antacids primarily composed of?

Salts of aluminum, magnesium, calcium, and/or sodium.

17
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What common antiflatulent drug is often included in antacid preparations?

Simethicone.

18
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What is a potential adverse effect of calcium antacids?

Kidney stones and increased gastric acid secretion (hyperacidity rebound).

19
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Which patients should avoid antacids containing magnesium?

Patients with renal failure due to potential accumulation of magnesium to toxic levels.

20
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How do antacids work?

They neutralize acid secretions in the stomach but do not prevent their overproduction.

21
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What are the indications for antacids?

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

22
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What is a common adverse effect of aluminum salt antacids?

Constipation.

23
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What is a common adverse effect of magnesium salt antacids?

Diarrhea.

24
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What adverse effect can sodium bicarbonate antacids cause in some patients?

Problems in patients with heart failure (HF), hypertension, or renal insufficiency due to its sodium content.

25
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For a patient with chronic renal failure, which type of antacid is generally the best choice?

An aluminum-containing antacid.

26
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What is the purpose of antiflatulents like simethicone?

To relieve the painful symptoms associated with gas.

27
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What are some general adverse effects of antacids?

Metabolic alkalosis (overuse), constipation (aluminum, calcium), diarrhea (magnesium), kidney stones (calcium), rebound hyperacidity (calcium), gas/belching (calcium carbonate).

28
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How do antacids affect the absorption of other drugs?

They can reduce the absorption of other drugs due to adsorption and chelation, forming insoluble complexes.

29
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What are some common Histamine 2 (H2) receptor antagonists?

Cimetidine (Tagamet), nizatidine (Axid), and famotidine (Pepcid).

30
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How do H2 receptor antagonists work?

They competitively block the H2 receptor of acid-producing parietal cells, reducing hydrogen ion secretion and increasing stomach pH.

31
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What are the indications for H2 antagonists?

Gastroesophageal reflux disease (GERD), PUD, erosive esophagitis, and as adjunct therapy to control upper GI bleeding.

32
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What are some common adverse effects of H2 antagonists?

Central nervous system effects (confusion, disorientation) in elderly patients, impotence and gynecomastia (cimetidine), and thrombocytopenia (famotidine).

33
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Why has cimetidine been largely replaced by other H2 antagonists?

It binds with the P-450 microsomal oxidase system in the liver, inhibiting the oxidation of many drugs and increasing their levels.

34
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What effect does smoking have on H2 blockers?

Smoking decreases their effectiveness.

35
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When should H2 receptor antagonists be taken relative to antacids for optimal results?

1 to 2 hours before antacids.

36
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What is the 'proton pump' in gastric acid production?

The process by which parietal cells release positive hydrogen ions (protons) during HCl production.

37
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Do H2 blockers stop the action of the proton pump?

No, H2 blockers and antihistamines do not stop the action of the proton pump.

38
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What are some common Proton Pump Inhibitors (PPIs)?

Lansoprazole (Prevacid), omeprazole (Prilosec), rabeprazole (AcipHex), pantoprazole (Protonix), and esomeprazole (Nexium).

39
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How do PPIs work?

They irreversibly bind to the H+/K+ ATPase enzyme, preventing hydrogen ion movement into the stomach and temporarily blocking all gastric acid secretion (achlorhydria).

40
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What are the indications for PPIs?

GERD, erosive esophagitis, short-term treatment of active duodenal and benign gastric ulcers, Zollinger-Ellison syndrome, NSAID-induced ulcers, stress ulcer prophylaxis, and H. pylori-induced ulcers (given with an antibiotic).

41
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What are some potential adverse effects of long-term PPI use?

Predisposition to GI tract infections (Clostridium difficile), osteoporosis with increased risk of wrist, hip, and spine fractures, pneumonia, and depletion of magnesium.

42
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What other drugs can PPIs interact with?

Diazepam and phenytoin (increased serum levels), warfarin (increased bleeding risk), ketoconazole, ampicillin, iron salts, and digoxin (decreased absorption), and clopidogrel. Food may also decrease PPI absorption.

43
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What are some miscellaneous acid-controlling drugs?

Sucralfate (Carafate), misoprostol (Cytotec), and simethicone (Mylicon).

44
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How does sucralfate (Carafate) work?

It is a cytoprotective drug that binds to the base of ulcers and erosions, forming a protective barrier against pepsin.

45
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What are some important considerations for administering sucralfate?

Little absorption from the gut, may cause constipation/nausea/dry mouth, may impair absorption of other drugs (give other drugs at least 2 hours before sucralfate), and binds with phosphate (useful in chronic renal failure).

46
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How does misoprostol (Cytotec) work?

It is a prostaglandin E analog that protects gastric mucosa by enhancing local mucus/bicarbonate production, promoting cell regeneration, and maintaining mucosal blood flow.

47
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What is misoprostol primarily used for?

Prevention of NSAID-induced gastric ulcers.

48
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How does simethicone work as an antiflatulent drug?

It alters the elasticity of mucus-coated gas bubbles, breaking them into smaller ones, leading to decreased gas pain and increased expulsion.

49
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What is an important nursing implication regarding antacid administration and other medications?

Most medications should be administered 1 to 2 hours after an antacid because antacids can reduce absorption or cause premature dissolving of enteric-coated medications.

50
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How should chewable antacid tablets be taken?

They should be chewed thoroughly, and liquid forms should be shaken well before giving.

51
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Why should antacids be administered with at least 8 oz of water?

To enhance absorption (except for rapid-dissolve forms).

52
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What is a caution for long-term self-medication with antacids?

It may mask symptoms of serious underlying diseases, such as malignancy or bleeding ulcers, requiring medical evaluation if symptoms persist.

53
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When should H2 antagonists be taken relative to antacids?

1 to 2 hours before antacids.

54
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What are some considerations for administering pantoprazole capsules via NG tube?

The NG tube must be at least 16 gauge, and capsule contents can be mixed with apple juice (do not chew or crush delayed-release granules).

55
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How is diarrhea defined?

Abnormal passage of stools with increased frequency, fluidity, and weight, or with increased stool water excretion.

56
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What is acute diarrhea?

Sudden onset in a previously healthy person, lasting from 3 days to 2 weeks, self-limiting, and resolving without sequelae.

57
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What is chronic diarrhea?

Lasts for more than 3 to 4 weeks, associated with recurring diarrheal stools, fever, loss of appetite, nausea, vomiting, weight loss, and chronic weakness.

58
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What are some common causes of acute diarrhea?

Bacteria, viruses, drug-induced factors, nutritional factors, and protozoa.

59
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What are some causes of chronic diarrhea?

Tumors, diabetes mellitus, Addison’s disease, hyperthyroidism, irritable bowel syndrome, and AIDS.

60
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What are the main goals of diarrhea treatment?

Stopping stool frequency, alleviating abdominal cramps, replenishing fluids and electrolytes, and preventing weight loss and nutritional deficits.

61
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What are the main types of antidiarrheal drugs?

Adsorbents, antimotility drugs (anticholinergics and opiates), and probiotics (intestinal flora modifiers).

62
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How do adsorbent antidiarrheals work?

They coat the walls of the GI tract and bind to causative bacteria or toxins, which are then eliminated through the stool.

63
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What are some examples of adsorbent antidiarrheals?

Bismuth subsalicylate (Pepto-Bismol), activated charcoal, colestipol, and cholestyramine.

64
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How do anticholinergic antidiarrheals work?

They decrease intestinal muscle tone and peristalsis of the GI tract, slowing the movement of fecal matter.

65
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How do opiate antidiarrheals work?

They decrease bowel motility, reduce pain, and decrease transit time, allowing more time for water and electrolytes to be absorbed.

66
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What are some examples of opiate antidiarrheals?

Paregoric, opium tincture, codeine, loperamide (OTC), and diphenoxylate.

67
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How do probiotics work as antidiarrheals?

They supply missing bacteria to the GI tract and suppress the growth of diarrhea-causing bacteria.

68
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When are different types of antidiarrheals indicated?

Adsorbents for milder cases, anticholinergics and opiates for more severe cases, and probiotics for antibiotic-induced diarrhea.

69
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What are some adverse effects of adsorbent antidiarrheals?

Increased bleeding time, constipation, dark stools, confusion, tinnitus, metallic taste, and blue tongue.

70
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What are some adverse effects of anticholinergic antidiarrheals?

Urinary retention, impotence, headache, dizziness, confusion, anxiety, drowsiness, dry skin, flushing, blurred vision, hypotension, and bradycardia.

71
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What are some adverse effects of opiate antidiarrheals?

Drowsiness, dizziness, lethargy, nausea, vomiting, constipation, respiratory depression, hypotension, urinary retention, and flushing.

72
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What drug interactions are associated with adsorbents?

They decrease the absorption of many drugs (e.g., digoxin, quinidine, hypoglycemic drugs), cause increased bleeding time and bruising with anticoagulants (warfarin), and increase toxic effects of methotrexate.

73
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In which patients should anticholinergics not be administered?

Patients with a history of narrow-angle glaucoma, GI obstruction, myasthenia gravis, paralytic ileus, or toxic megacolon.

74
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What nursing implications are important for patients taking antidiarrheals?

Teach patients to take medications exactly as prescribed, be aware of fluid intake and dietary changes, assess fluid volume status, input and output, and mucous membranes, and notify prescribers if symptoms persist.

75
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How is constipation defined?

Abnormally infrequent and difficult passage of feces through the lower GI tract.

76
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Is constipation a disease?

It is a symptom, not a disease.

77
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What are the non-surgical treatments for constipation?

Dietary (e.g., fiber supplementation), behavioral (e.g., increased physical activity), and pharmacologic.

78
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What are the main types of laxatives?

Bulk forming, emollient (stool softeners, lubricant laxatives), hyperosmotic, saline, and stimulant.

79
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How do bulk-forming laxatives work?

They absorb water to increase bulk and distend the bowel to initiate reflex bowel activity.

80
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What are examples of bulk-forming laxatives?

Psyllium (Metamucil) and methylcellulose (Citrucel).

81
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How do emollient laxatives work?

They are stool softeners and lubricants that promote more water and fat in the stools, and lubricate the fecal material and intestinal walls.

82
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What are examples of emollient laxatives?

Docusate salts (Colace, Surfak) and mineral oil.

83
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How do hyperosmotic laxatives work?

They increase fecal water content, resulting in bowel distention, increased peristalsis, and evacuation.

84
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What are examples of hyperosmotic laxatives?

Polyethylene glycol (PEG), sorbitol, glycerin, and lactulose.

85
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What is an additional use for lactulose?

To reduce elevated serum ammonia levels.

86
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How do saline laxatives work?

They increase osmotic pressure within the intestinal tract, causing more water to enter, which results in bowel distention, increased peristalsis, and evacuation.

87
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What are examples of saline laxatives?

Magnesium hydroxide (Milk of Magnesia) and magnesium citrate (Citroma).

88
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How do stimulant laxatives work?

They increase peristalsis via intestinal nerve stimulation.

89
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What are examples of stimulant laxatives?

Senna (Senokot) and bisacodyl (Dulcolax).

90
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What are peripherally acting opioid antagonists used for?

Treatment of constipation related to opioid use and bowel resection therapy.

91
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What are some general adverse effects of laxatives?

Impaction, fluid disturbances, electrolyte imbalances, esophageal blockage (bulk forming), skin rashes, decreased absorption of vitamins, lipid pneumonia (emollient), abdominal bloating, rectal irritation (hyperosmotic), magnesium toxicity, cramping, increased thirst (saline), nutrient malabsorption, gastric irritation, discolored urine (stimulant), and electrolyte imbalances (all types).

92
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What non-pharmacological interventions should be encouraged as alternatives to laxative use?

A healthy, high-fiber diet and increased fluid intake.

93
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What is a risk of long-term laxative use?

Decreased bowel tone and potential dependency.

94
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How should laxative tablets be swallowed?

Whole, not crushed or chewed, especially if enteric coated.

95
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How should bisacodyl be administered?

With water, avoiding milk, antacids, and juices due to interactions.

96
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What symptoms should patients report to their prescribers when taking laxatives?

Severe abdominal pain, muscle weakness, cramps, or dizziness, which may indicate fluid or electrolyte loss.

97
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What is Irritable Bowel Syndrome (IBS) characterized by?

Chronic intestinal discomfort with cramps, diarrhea, or constipation.

98
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What are some drugs used to treat IBS with diarrhea (IBS-D)?

Alosetron (Lotronex), rifaximin (Xifaxan), and eluxadoline (Viberzi).

99
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What are some drugs used to treat IBS with constipation (IBS-C)?

Lubiprostone (Amitiza) and linacotide (Linzess).

100
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What is nausea?

An unpleasant feeling that often precedes vomiting.