Gastric acid action

Biologica.1 Activities a.ndAna.logues, The many pharmacological actions of neurotensin include hypotension, increased vascular permeabihty, hyperglycemia, increased intestinal motility, and inhibition of gastric acid secretion (120). In the brain, it produces analgesia at remarkably low doses (121). 

CCK is found in the digestive tract and the central and peripheral nervous systems. In the brain, CCK coexists with DA. In the peripheral nervous system, the two principal physiological actions of CCK are stimulation of gaU. bladder contraction and pancreatic enzyme secretion. CCK also stimulates glucose and amino acid transport, protein and DNA synthesis, and pancreatic hormone secretion. In the CNS, CCK induces hypothermia, analgesia, hyperglycemia, stimulation of pituitary hormone release, and a decrease in exploratory behavior. The CCK family of neuropeptides has been impHcated in anxiety and panic disorders, psychoses, satiety, and gastric acid and pancreatic enzyme secretions. 

These drug inhibit die action of histamine at histamine H2 receptor cells of die stomach, which then reduces die secretion of gastric acid and reduces total pepsin output. The decrease in acid allows the ulcerated areas to heal. Examples of histamine H2 antagonists include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid Pulvules), ranitidine (Zantac). 

Few peptide bonds that are hydrolyzed by proteolytic enzymes are accessible without prior denaturation of dietary proteins (by heat in cooking and by the action of gastric acid). 

The anti-ulcer agents omeprazole, lanzoprazole, and pantoprazole have been introduced during the past decade for the treatment of peptic ulcers. Gastric acid secretion is efficiently reduced by prazole inhibition of H+K+-ATPase in the parietal cells of the gastrointestinal mucosa [75]. The prazoles themselves are not active inhibitors of the enzyme, but are transformed to cyclic sulfenamides in the intracellular acidic compartment of parietal cells [76]. The active inhibitors are permanent cations at pH < 4, with limited possibilities of leaving the parietal cells, and thus are retained and activated at the site of action. In the neutral body compartments the prazoles are stable, and only trace amounts are converted to the active drugs. (For a review on omeprazole, see Ref. [77].)... 

Increases gastric acidity by preventing the action of inhibitory guanine nucleotide-binding protein (G protein) on adenylate cyclase... 

The answer is d. (Hardman 7 pp 907—909J The main action of omeprazole is the inhibition of secretion of gastric acid Because it is a specific inhibitor of the proton pump (H+,K+,ATPase), other actions are secondary to the marked decline of acid secretion. As a result of the reduction of gastric acidity, there is increased secretion of gastrin leading to hyper-gastrinemia. 

Alginic Acid + Aluminum Hydroxide Magnesium Tnsilicate (Gaviscon) [Antacid] [OTC] Uses Heartburn hiatal hernia pain Action Protective layer blocks gastric acid Dose 2—4- tabs or 15-30 mL PO qid followed by H2O Caution [B, -] Avoid in renal impair or Na -restricted diet Disp Tabs, susp SE D, constipation Interactions T Absorption OF tetracyclines EMS None OD May cause constipation, loss of appetite, muscle weakness, and peripheral edema symptomatic and supportive... 

Aluminum Hydroxide + Magnesium Carbonate (Gaviscon Extra Strength/ Liquid) [OTC] [Antacid/Aluminum Magnesium Salts] Uses Relief of heartburn, acid indigestion Action Neutralizes gastric acid Dose Adults. 15-30 mL PO pc hs Peds. 5-15 mL PO qid or PRN avoid in renal impair Caution T Mg (w/ renal insuff) [C, ] Disp Liq, chew tabs SE Constipation, D Interactions In addition to AlOH effects OF histamine blockers, hydantoins, nitrofurantoin, phenothiazines, ticlopidine, T effects OF... 

Calcium Acetate (PhosLo) [Calcium Supplement/ Anti arrhythmic/Mmeral/ Electrolyte] Uses ESRD-associated hyper-phos-phatemia Action Ca " supl w/o aluminum to X P04 absorption Dose 2-4 tabs PO w/ meals Caution [C, ] Contra t Ca Disp Gelcap SE Can t Ca, hypophosphatemia, constipation Interactions t Effects OF quinidine X effects W/ large intake of dietary fiber, spinach, rhubarb X effects OF atenolol, CCB, etidronate, tetracyclines, fluoroquinolones, phenytoin, Fe salts, thyroid hormones EMS Pts have reduced renal Fxn, monitor ECG for signs of electrolyte disturbances OD S/Sxs of hypercalcemia (confusion, weakness, GI upset, constipation, N, V, and cardiac arrhythmias) give IV fluid for diuresis symptomatic and supportive Calcium Carbonate (TumS/ Alka Mints) [Antacid/ Calcium Supplement/Mineral/ Electrolyte] [OTC] Uses Hyperacidity associated w/ peptic ulcer Dz, hiatal hernia, etc Action Neutralizes gastric acid Dose 500 mg—2 g PO PRN -1- in renal impair Caution [C, ] Disp Chew tabs, susp SE t -1- PO constipation Interactions X Effect OF tetracyclines, fluo-... 

Esomeprazole (Nexium) [Gastric Acid Inhibitor/Proton Pump Inhibitor] Uses Short-term (4-8 wk) for erosive esophagitis/GERD H. pylori Infxn in combo w/ antibiotics Action Proton pump inhibitor, gastric acid Dose Adults. GERD/erosive gastritis 20 0 mg/d PO x 4-8 wk 20 0 mg IV 10-30 min inf or >3 min IV push, 10 d max Maint 20 mg/d... 

Pantoprazole (Protonix) [Gastric Acid Suppressant/Proton Pump Inhibitor] Uses GERD, erosive gastritis, ZE synd, PUD Action Proton pump inhibitor Dose 40 mg/d PO do not crush/chew tabs 40 mg IV/d (not >3 mg/min, use Protonix filter) Caution [B, /-] Disp Tabs, inj SE Chest pain, anxiety, GI upset Interactions t Effects OF warfarin t effects of photosensitivity W/ St. John s wort X effects OF ketoconazole EMS t Effects of anticoagulants may affect glucose (hypoglycemia) OD Unlikely to cause life-threatening Sxs... 

Secretory actions Tendency to increased Stimulate secretion of gastric acid and... 

Agents in this class are omeprazole, lansoprazole, pantoprazole and rabeprazole. Esomeprazole is the S-enantiomer of omeprazole. After ingestion of gastric acid resistant formulations they are rapidly and more or less completely absorbed. Bioavailability may be reduced if administered with food or antacids. Elimination is via metabolism in the liver and the renal excretion of inactive metabolites. The elimination half-live is very variable, however, as explained above, not related to the duration of action. 

Nonselective antimuscarinic drugs have been employed in the therapy of peptic ulcers (see Chapter 40) because they can reduce gastric acid secretion they also have been used as adjunctive therapy in the treatment of irritable bowel syndrome. Antimuscarinic drugs can decrease the pain associated with postprandial spasm of intestinal smooth muscle by blocking contractile responses to ACh. Some of the agents used for this disorder have only antimuscarinic activity (e.g., propantheline), while other drugs have additional properties that contribute to their antispasmodic action. Dicyclomine (Bentyl) and oxybutynin (Ditropan) at therapeutic concentrations primarily have a direct smooth muscle relaxant effect with little antimuscarinic action. 

Mechanism of Action An antacid that reduces gastric acid by binding with phosphate in the intestine, and then is excreted as aluminum carbonate in feces. Aluminum carbonate may increase the absorption of calcium due to decreased serum phosphate levels. The drug also has astringent and adsorbent properties. Therapeutic Effect Neutralizes or increases gastric pH reduces phosphates in urine, preventing formation of phosphate urinary stones reduces serum phosphate levels decreases fluidity of stools. 

Mechanism of Action An electrolyte that is essential for the function and integrity of the nervous, muscular, and skeletal systems. Calcium plays an important role in normal cardiac and renal function, respiration, blood coagulation, and cell membrane and capillary permeability. It helps regulate the release and storage of neurotransmitters and hormones, and it neutralizes or reduces gastric acid (increase pH). Calcium acetate combines with dietary phosphate to form insoluble calcium phosphate. Therapeutic Effect Replaces calcium in deficiency states controls hyperphosphatemia in end-stage renal disease. 

Mechanism of Action Aproton pump inhibitor that is converted to active metabolites that irreversibly bind to and inhibit hydrogen-potassium adenosine triphosphates, an enzyme on the surface of gastricparietal cells. Inhibits hydrogen ion transport into gastric lumen. Therapeutic Effect Increases gastricpH, reducing gastric acid production. 

Mecftanism of Action AGI Hj-blocker and gastric acid secretion inhibitor that inhibits histamine action at histamine 2 receptors of parietal cells Therapeutic Effect Inhibits gastric acid secretion when fasting, at night, or when stimulated by food, caffeine, or insulin. 

Mechanism of Action A proton pump inhibitor that selectively Inhibits the parietal cell membrane enzyme system (hydrogen-potassium adenosine triphosphatase) or proton pump. Therapeutic Effect Suppresses gastric acid secretion. Pharmacokinetics ... 

Mechanism of Action A prostaglandin that inhibits basal, nocturnal gastric acid secretion via direct action on parietal cells. Therapeutic Effect Increases production of protective gastric mucus. 

Mechanism of Action An antiulcer agent that forms an ulcer-adherent complex with proteinaceous exudate, such as albumin, at ulcer site. Also forms a viscous, adhesive barrier on the surface of intact mucosa of the stomach or duodenum. Therapeutic Effect Protects damaged mucosa from further destruction by absorbing gastric acid, pepsin, and bile salts. 

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