Chapter 50: Acid-Controlling Flashcards
• One stomach condition requiring drug therapy
hyperacidity, or excessive acid production. Left untreated, hyperacidity can lead to serious conditions such as acid reflux, ulcer disease, esophageal damage, and even esophageal cancer.
• The stomach secretes many substances
(hydrochloric acid, pepsinogen, mucus, bicarbonate, intrinsic factor, and prostaglandins).
• The gastric glands are highly specialized secretory glands composed of several different types of cells
parietal, chief, mucous, endocrine, and enterochromaffin.
- Parietal cells produce and secrete hydrochloric acid (HCl). They are the primary site of action for many of the drugs used to treat acid-related disorders.
- Chief cells secrete pepsinogen. Pepsinogen is a proenzyme (enzyme precursor) that becomes pepsin when activated by exposure to acid. Pepsin breaks down proteins and is therefore referred to as a proteolytic enzyme.
- Mucous cells are mucus-secreting cells that are also called surface epithelial cells. The secreted mucus serves as a protective coating against the digestive action of HCl and digestive enzymes
• When the balance of these cells and secretions is impaired, acid-related diseases can occur.
• The most harmful of the acid-related diseases involve hypersecretion of acid and include peptic ulcer disease and esophageal cancer. The most common condition is mild to moderate hyperacidity.
• Hyperacidity is often associated with gastroesophageal reflux disease (GERD).
This is the tendency of excessive and acidic stomach contents to back up, or reflux, into the lower (and even upper) esophagus. Over time, this condition can lead to more serious disorders such as erosive esophagitis and Barrett esophagus, a precancerous condition.
• Several substances stimulate HCl secretion by the parietal cells, such as food, caffeine, chocolate, and alcohol. In moderation, any of these is usually not problematic
• Excessive consumption of large, fatty meals or alcohol, as well as emotional stress, may result in hyperproduction of HCl and lead to hypersecretory disorders such as peptic ulcer disease.
acid-peptic disorders.
• Because the process of ulceration is driven by the proteolytic (protein breakdown) actions of pepsin together with the caustic effects of HCl, peptic ulcer disease and related problems are also referred to by the more general term acid-peptic disorders
• H. pylori is found in the GI tracts of roughly 90% of patients with duodenal ulcers and 70% of those with gastric ulcers.
. First-line therapy includes a 10- to 14-day course of a proton pump inhibitor and the antibiotics clarithromycin and either amoxicillin or metronidazole.
• GI lesions are common in ICU patients, especially in the 24 hours after admission
Factors include decreased blood flow, mucosal ischemia, hypoperfusion, and reperfusion injury. Guidelines suggest that all such patients receive either a histamine receptor–blocking drug or a proton pump inhibitor.
• Adverse effects of antacids are limited
Magnesium preparations, such as milk of magnesia, can cause diarrhea. Aluminum- and calcium-containing formulations can cause constipation
• Antacids are basic compounds used to neutralize stomach acid.
Most commonly they are nonprescription salts of aluminum, magnesium, calcium, and/or sodium
- Many drug interactions occur with the acid-controlling drugs due to alteration of oral dosage forms, and so other medications are to be avoided within 1 to 2 hours of taking an antacid. Antacids are sometimes to be avoided when other acid-controlling drugs are taken
- Significant patient harm may ensue when the quinolone antibiotics (ciprofloxacin, levofloxacin, moxifloxacin) are given with antacids.
• Four basic mechanisms by which antacids cause interactions include adsorption of other drugs to antacids, which reduces the ability of the 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 the absorption of acidic drugs; and increased urinary pH, which increases the excretion of acidic drugs and decreases the excretion of basic drugs.
• H2 receptor antagonists, also known as H2RAs and H2 receptor blockers, are the prototypical acid-secretion antagonists.
They are H2 blockers that bind to and block histamine receptors located on parietal cells. Up to 90% inhibition of acid secretion can be achieved
• The effect of reduced hydrogen ion secretion from the parietal cells results in an increase in the stomach pH and relief of symptoms associated with hyperacidity-related conditions.
- H2 receptor antagonists are used for
* The H2 receptor antagonists include the drugs cimetidine, ranitidine, famotidine, and nizatidine.
for GERD, peptic ulcer disease, and erosive esophagitis; adjunct therapy in the control of upper GI tract bleeding; and treatment of pathologic gastric hypersecretory conditions such as Zollinger-Ellison syndrome
• Cimetidine carries a higher risk of drug interactions than ranitidine, famotidine, and nizatidine, especially in elderly.
Cimetidine binds enzymes of the hepatic cytochrome P-450 microsomal oxidase system, liver enzymes that metabolize many different drugs. By inhibiting the metabolism of drugs metabolized via this pathway, it may raise the blood concentrations of certain drugs.
