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Adv Pharm > Chapter 64: Peptic Ulcer Disease > Flashcards

Chapter 64: Peptic Ulcer Disease Flashcards

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

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

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
Q

Metronidazole [Flagyl]

A

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
Q

​Tinidazole [Tindamax]

A

Very similar to metronidazole
Has the same adverse effects and interactions

Can cause a disulfiram-like reaction

Do not combine with alcohol

27
Q

Histamine2 Receptor Antagonists

A

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
Q

Cimetidine [Tagamet] pharmacokinetics

A

Absorption is slowed if taken with meals

Crosses the blood-brain barrier with difficulty

May cause some CNS side effects

29
Q

Cimetidine [Tagamet] therapeutic uses

A

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
Q

Tagamet ADR

A

Antiandrogenic effects

CNS effects

Pneumonia

IV bolus: Can cause hypotension and dysrhythmias

31
Q

Tagamet drug interactions

A

Warfarin, phenytoin, theophylline, lidocaine

Antacids can reduce absorption of cimetidine
Cimetidine and antacids should be administered at least 1 hour apart

32
Q

Ranitidine [Zantac]

A

Has many of the properties of cimetidine

More potent, fewer adverse effects, fewer drug interactions than cimetidine

33
Q

Zantac ADR

A

Significant ones are uncommon

Does not bind to androgen receptors

Elevation of gastric pH may increase the risk of pneumonia

34
Q

Zantac therapeutic uses

A

Short-term treatment of gastric/duodenal ulcers

Prophylaxis of recurrent duodenal ulcers

Treatment of Zollinger-Ellison syndrome and hypersecretory states

Treatment of GERD

35
Q

Famotidine [Pepcid]

A

Actions similar to those of ranitidine

36
Q

Pepcid uses

A

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
Q

Pepcid ADR

A

No antiandrogenic effects because it does not bind to androgen receptors

Possible increased risk for pneumonia caused by elevation of pH

38
Q

Nizatidine [Axid]

A

Actions much like those of ranitidine and famotidine

Therapeutic uses
Duodenal/gastric ulcers
GERD, heartburn, acid indigestion, sour stomach

39
Q

Proton Pump Inhibitors

A

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
Q

Omeprazole [Prilosec] actions

A

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
Q

Prilosec ADR

A

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
Q

Esomeprazole [Nexium, Nexium I.V.]

A

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
Q

Lansoprazole [Prevacid, Prevacid IV, Prevacid 24 HR]

A

Very similar to omeprazole

Adverse effects: Diarrhea, abdominal pain, nausea, pneumonia, hypomagnesemia, osteoporosis, fracture

44
Q

Dexlansoprazole [Dexilant]

A

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
Q

Rabeprazole

A

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
Q

Pantoprazole [Protonix]

A

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
Q

Other anti ulcer drugs

A

Sucralfate [Carafate]
Misoprostol [Cytotec]
Antacids

48
Q

Sucralfate [Carafate]

A

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
Q

Misoprostol [Cytotec]

A

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
Q

Antacids

A

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

51
Q

Antacid Families

A

Aluminum compounds

Magnesium compounds

Calcium compounds

Sodium compounds

52
Q

Magnesium Hydroxide [Milk of Magnesia]

A

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
Q

Aluminum Hydroxide

A

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
Q

Calcium Carbonate

A

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
Q

Sodium Bicarbonate

A

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
Q

Combo packs

A

Helidac
Pylera
Prevpac

Adv Pharm (76 decks)

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