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Adv Pharm > Chapter 64: Peptic Ulcer Disease > Flashcards

Chapter 64: Peptic Ulcer Disease Flashcards

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1
Q

PUD

A

Group of upper gastrointestinal (GI) disorders

Degrees of erosion of the gut wall

Severe erosion can be complicated by hemorrhage and perforation

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2
Q

PUD causes

A

Imbalance between mucosal and aggressive factors

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3
Q

Gastric defensive factors

A

Mucus
Secreted cells of the GI mucosa
Forms a barrier to protect underlying cells from acid and pepsin

Bicarbonate
Secreted by epithelial cells of stomach and duodenum
Most remains trapped in mucus layer to neutralize hydrogen ions that penetrate the mucus

Blood flow
Poor blood flow can lead to ischemia, cell injury, and vulnerability to attack

Prostaglandins
Stimulate the secretion of mucus and bicarbonate

*NSAIDs and H pylori are 2 major agents that weaken defensive mechanism

*mucous and bicarbonate are major defensive mechanisms

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4
Q

Aggressive factors of PUD: H pylori

A

Helicobacter pylori, also known as H. pylori
Gram-negative bacillus that can colonize the stomach and duodenum

Lives between epithelial cells and the mucus barrier
Escapes destruction by acid

Can remain in the GI tract for decades

Half of the world is infected, but most people do not develop symptomatic peptic ulcer disease (PUD)

60% to 70% of patients with PUD have H. pylori infection

H. pylori may also promote gastric cancer

Duodenal ulcers are much more common among people with H. pylori infection than among people who are not infected

Eradication of the bacterium promotes healing of the PUD and minimized recurrence of PUD

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5
Q

Aggressive factors of PUD : NSAIDs

A

Inhibit the biosynthesis of prostaglandins

Reduce blood flow, mucus, and bicarbonate

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6
Q

Aggressive factors of PUD: gastric acid

A

Causes ulcers directly by injuring cells of the GI mucosa and indirectly by activating pepsin

Increased acid alone does not increase ulcers but is a definite factor in PUD

Zollinger-Ellison syndrome

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7
Q

Pathogenesis of PUD: pepsin

A

Proteolytic enzyme in gastric juice

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8
Q

Pathogenesis of PUD: smoking

A

Delays ulcer healing and increases risk for recurrence

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9
Q

Summary of ulcer development

A

Most common cause
Infection with H. pylori is the most common cause of gastric and duodenal ulcers
Additional factors must be involved; 50% harbor H. pylori, but only 10% develop PUD

Second most common cause
NSAIDs

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10
Q

Overview of tx for PUD

A

Goals of drug therapy
Alleviate symptoms
Promote healing
Prevent complications
Prevent recurrence

Drugs do not alter the disease process; they create conditions conducive to healing

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11
Q

Classes of Antiulcer Drugs

A

Antibiotics

Antisecretory agents

Mucosal protectants

Antisecretory agents that enhance mucosal defenses

Antacids

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12
Q

Three Ways Antiulcer Drugs Work

A
  1. Eradicate H pylori -antibiotics
  2. Reduce gastric acidity -anti secretory agents, misprostol
  3. Enhance mucosal defenses -sucralfate, misoprostol
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13
Q

H pylori ulcers drug selection

A

Antibiotics
Should be given to all patients with gastric/duodenal ulcers and documented H. pylori infection

Antisecretory agents

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14
Q

NSAID-induced ulcer drug selection

A

Prophylaxis:
Risk factors for ulcer development: Age over 60 years, history of ulcers, high-dose NSAID therapy
Proton pump inhibitors (PPIs) are preferred (e.g., omeprazole)
Misoprostol is also effective but can cause diarrhea

Treatment
Histamine blockers and PPIs (e.g., omeprazole) are preferred
Antacids, sucralfate, and histamine2 receptor blockers are not recommended
Discontinue NSAIDs if possible

Evaluation of treatment
Monitor for relief of pain, endoscopic exams, check for H pylori in stools

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15
Q

Pepsin

A

Proteolytic enzyme that can contribute to ulcer formation; it promotes ulcers by breaking down protein in the gut wall

Activity of pepsin is pH dependent; drugs that elevate gastric pH (e.g., antacids, histamine2 antagonists, PPIs) can cause peptic activity to increase, thereby enhancing pepsin’s destructive effects

To avoid activation of pepsin, drugs that reduce acidity should be administered in doses sufficient to raise the gastric pH above 5

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16
Q

Non drug ulcer therapy

A

Diet
Traditional “ulcer diet” does not accelerate healing
No convincing evidence indicates that caffeinated beverages promote ulcers or delay healing
Change in eating pattern to five or six small meals a day reduces pH fluctuations

Avoid smoking, aspirin, other NSAIDs, and alcohol

Stress reduction

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17
Q

Evaluation of Therapy for ulcers

A

Monitor for relief of pain
Keep in mind: Cessation of pain and disappearance of ulcer rarely coincide
Pain may subside before complete healing or may continue after healing

Radiologic or endoscopic examination of ulcer site

H. pylori tests

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18
Q

H pylori tests

A

Noninvasive
Breath test
Serologic test
Stool test

Invasive
Endoscopic specimen obtained and evaluated
Stained and viewed under microscope to see if H. pylori is present
Assayed for the presence of urease (a marker enzyme for H. pylori)
Cultured and then assayed for the presence of H. pylori

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19
Q

H pylori tx

A

Minimum of two antibiotics prescribed (up to three may be used) to reduce risk of resistance developing
Amoxicillin
Clarithromycin
Bismuth compounds
Tetracycline
Metronidazole
Tinidazole

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20
Q

Antibiotic Regimen for h pylori

A

Clarithromycin (if the area doesn’t have high resistance), amoxicillin, bismuth, metronidazole, and tetracycline

None is effective alone
Want them in combination

If these drugs are used alone, the risk of resistance developing increases

Goal: Minimize emergence of resistance; guidelines recommend using at least two antibiotics, preferably three

Antisecretory agent: PPI or histamine2 receptor antagonist (H2RA) also should be used

Eradication rates are good with a 10-day course and slightly better with a 14-day course

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21
Q

Clarithromycin [Biaxin]

A

Suppresses the growth of H. pylori by inhibiting protein synthesis

In the absence of resistance, treatment is highly effective

Unfortunately, rate of resistance is rising, exceeding 20% in some areas

Most common side effects
Nausea
Diarrhea
Distortion of taste

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22
Q

Amoxicillin

A

H. pylori is highly sensitive to amoxicillin

Rate of resistance is low, only about 3%

Amoxicillin kills bacteria by disrupting cell wall

Antibacterial activity is highest at a neutral pH and thus can be enhanced by reducing gastric acidity with an antisecretory agent (e.g., omeprazole)

Most common side effect is diarrhea

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23
Q

Bismuth Compounds

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A

Act topically to disrupt the cell wall of H. pylori, causing lysis and death

Also may inhibit urease activity and may prevent H. pylori from adhering to the gastric surface

Can impart a harmless black coloration to the tongue and stool
Patient teaching

Long-term therapy: Possible risk of neurologic injury

24
Q

Tetracycline

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A

Inhibitor of bacterial protein synthesis

Highly active against H. pylori

Resistance is rare (less than 1%)

Do not use in pregnant patients and young children because tetracycline can stain developing teeth

25
Metronidazole [Flagyl]
Very effective against sensitive strains of H. pylori Over 40% of strains are now resistant Most common side effects are nausea and headache Avoid alcohol: Disulfiram-like reaction can occur if metronidazole is used with alcohol Avoid use during pregnancy
26
​Tinidazole [Tindamax]
Very similar to metronidazole Has the same adverse effects and interactions Can cause a disulfiram-like reaction Do not combine with alcohol
27
Histamine2 Receptor Antagonists
Cimetidine [Tagamet] Ranitidine [Zantac] Famotidine [Pepcid] Nizatidine [Axid] All OTC Typically, when someone presents with PUD, they have tried one, if not many of these before they seek medical tx First-choice drugs for treating gastric and duodenal ulcers Promote healing by suppressing secretion of gastric acid All four are equally effective Serious side effects are uncommon
28
Cimetidine [Tagamet] pharmacokinetics
Absorption is slowed if taken with meals Crosses the blood-brain barrier with difficulty May cause some CNS side effects
29
Cimetidine [Tagamet] therapeutic uses
Gastric and duodenal ulcers Gastroesophageal reflux disease (GERD) Zollinger-Ellison syndrome Hypersecretion of gastric secretions lead to PU Aspiration pneumonitis Heartburn, acid indigestion, sour stomach
30
Tagamet ADR
Antiandrogenic effects CNS effects Pneumonia IV bolus: Can cause hypotension and dysrhythmias
31
Tagamet drug interactions
Warfarin, phenytoin, theophylline, lidocaine Antacids can reduce absorption of cimetidine Cimetidine and antacids should be administered at least 1 hour apart
32
Ranitidine [Zantac]
Has many of the properties of cimetidine More potent, fewer adverse effects, fewer drug interactions than cimetidine
33
Zantac ADR
Significant ones are uncommon Does not bind to androgen receptors Elevation of gastric pH may increase the risk of pneumonia
34
Zantac therapeutic uses
Short-term treatment of gastric/duodenal ulcers Prophylaxis of recurrent duodenal ulcers Treatment of Zollinger-Ellison syndrome and hypersecretory states Treatment of GERD
35
Famotidine [Pepcid]
Actions similar to those of ranitidine
36
Pepcid uses
Short-term treatment of gastric/duodenal ulcers Prophylaxis of recurrent duodenal ulcers Treatment of Zollinger-Ellison syndrome and hypersecretory states Treatment of GERD Over-the-counter (OTC): Treatment of heartburn, acid indigestion, sour stomach
37
Pepcid ADR
No antiandrogenic effects because it does not bind to androgen receptors Possible increased risk for pneumonia caused by elevation of pH
38
Nizatidine [Axid]
Actions much like those of ranitidine and famotidine Therapeutic uses Duodenal/gastric ulcers GERD, heartburn, acid indigestion, sour stomach
39
Proton Pump Inhibitors
Most effective drugs for suppressing secretion of gastric acid Therapeutic uses: Short term Gastric/duodenal ulcers GERD Well tolerated Selection of PPI is based on cost and prescriber’s preference Can increase the risk of serious adverse events, including fracture, pneumonia, acid rebound, and possibly intestinal infection with Clostridium difficile
40
Omeprazole [Prilosec] actions
First available PPI Actions and characteristics; Inhibits gastric secretion Short half-life Used for short-term therapy Ulcer prophylaxis is indicated only for patients in intensive care units, and then only if they have an additional risk factor, such as multiple trauma, spinal cord injury, or prolonged mechanical ventilation (longer than 48 hr) 30 mg dose will decrease acid production by 90-97% in 2 hr
41
Prilosec ADR
Usually inconsequential with short-term use Headache GI effects Pneumonia Fractures Hypomagnesemia Rebound acid hypersecretion C. difficile infection Gastric cancer Barrett’s esophagitis and that’s precancous For PUD, when med is d/c, can easily get a reoccurrence of the ulcer HA an GI SE are minimal
42
Esomeprazole [Nexium, Nexium I.V.]
Nearly identical to omeprazole [Prilosec] Uses: Erosive esophagitis, GERD, duodenal ulcers associated with H. pylori infection, prophylaxis of NSAID-induced ulcers Adverse effects: Headache, diarrhea, nausea, flatulence, abdominal pain, dry mouth, pneumonia, hypomagnesemia, osteoporosis, fractures
43
Lansoprazole [Prevacid, Prevacid IV, Prevacid 24 HR]
Very similar to omeprazole Adverse effects: Diarrhea, abdominal pain, nausea, pneumonia, hypomagnesemia, osteoporosis, fracture
44
Dexlansoprazole [Dexilant]
Reduces gastric acidity by inhibiting gastric H+,K+-ATPase Uses: Treatment and maintenance of healing of erosive esophagitis; treatment of symptomatic GERD (heartburn) Adverse effects: Diarrhea, abdominal pain, nausea, vomiting, flatulence, upper respiratory infection, hypomagnesemia, osteoporosis, fractures Used much less than others
45
Rabeprazole
Much like omeprazole and lansoprazole in actions, uses, and adverse effects Uses: H. pylori eradication, duodenal ulcers, GERD, hypersecretory states (e.g., Zollinger-Ellison syndrome) Mechanism of action: Reduces gastric acidity by inhibiting gastric H+,K+-ATPase
46
Pantoprazole [Protonix]
Similar to omeprazole and the other PPIs Uses: Treatment of GERD and hypersecretory states Adverse effects Oral: Diarrhea, headache, dizziness IV: Diarrhea, headache, nausea, dyspepsia, injection-site reactions, including thrombophlebitis and abscess Long-term use: Hypomagnesemia, osteoporosis, fractures
47
Other anti ulcer drugs
Sucralfate [Carafate] Misoprostol [Cytotec] Antacids
48
Sucralfate [Carafate]
Creates a protective barrier for up to 6 hours Therapeutic uses Acute ulcers and maintenance therapy Adverse effects Constipation (only 2% of patients) Drug interactions Minimal Antacids may interfere with effects of sucralfate
49
Misoprostol [Cytotec]
Therapeutic uses Only approved GI indication is prevention of gastric ulcers caused by long-term NSAID therapy Adverse effects Most common: Dose-related diarrhea and abdominal pain Contraindicated during pregnancy: Category X Significant actions need to be taken to ensure that pregnancy does not occur after therapy starts and that patient is not pregnant at therapy initiation
50
Antacids
React with gastric acid to produce neutral salts or salts of low acidity Reduce destruction of gut wall by neutralizing acid May also enhance mucosal protection by stimulating production of prostaglandins Except for sodium bicarbonate, antacids do not alter systemic pH Use with caution in patients with renal impairment Adverse effects Constipation: Aluminum hydroxide Diarrhea: Magnesium hydroxide Sodium loading Drug interactions Cimetidine Ranitidine Sucralfate
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Antacid Families
Aluminum compounds Magnesium compounds Calcium compounds Sodium compounds
52
Magnesium Hydroxide [Milk of Magnesia]
Rapid-acting, high acid-neutralizing capacity (ANC), produces long-lasting effects An antacid of choice Most prominent adverse effect is diarrhea Usually taken in combination with aluminum hydroxide, an antacid that promotes constipation Avoided in patients with undiagnosed abdominal pain Frequently used as a laxative Use with caution in patients with renal failure
53
Aluminum Hydroxide
Relatively low ANC, slow acting Effects have long duration Rarely used alone Widely used in combination with magnesium hydroxide Caution: Significant amounts of sodium Constipation Drug interactions: Tetracyclines, warfarin, digoxin
54
Calcium Carbonate
Rapid-acting, high ANC, effects have long duration Acid rebound Principal adverse effect: Constipation, which can be overcome by combining calcium carbonate with a magnesium-containing antacid (e.g., magnesium hydroxide) Eructation (belching) and flatulence Low palatability
55
Sodium Bicarbonate
Useful for treating acidosis and elevating urinary pH to promote excretion of acidic drugs after overdose Inappropriate for treating PUD: Brief duration, high sodium content, can cause alkalosis Eructation and flatulence Can exacerbate hypertension and heart failure Can cause systemic alkalosis in patients with renal impairment
56
Combo packs
Helidac Pylera Prevpac

Adv Pharm (76 decks)

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