Pharm-histamine exam 4/2
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Created by:
Rnkimmyjo Plus on February 5, 2011
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33 terms
Terms | Definitions |
|---|---|
 What are the effects of histamine release? | Produces a variety of physiologic and pathologic responses in different tissues. Acts as a mediator for inflammation for inflammation in allergic disease. Cause an increased capillary permeability, hypotension, tachycardia, flushing, and HA. |
| What are the different histamine receptors? | H1, H2, H3. |
| What effect does histamine have on the CV system? | Causes dilation of arterioles and capillaries leading to flushing, ↓ in PVR, ↓ in systemic BP, ↑capillary permeability. Positive chronotropic effects and cardiac dysrhythmias. |
| What effect does histamine have on airways? | Histamine activates H1 receptors to constrict bronchial smooth muscle. |
| What patients are more likely to develop increase in airway resistance in response to histamine? | Patients with obstructive airway disease, such as asthma and bronchitis. |
| What effect does histamine have on the GI system? | Histamine stimulates the release of copious secretions of gastric fluid containing high concentrations of hydrogen ions. Vagal activity results in higher rate of hydrogen ion secretion. |
| What are the clinical uses of histamine? | Assesses the ability of gastric parietal cells to secret hydrogen ions and to determine parietal cell mass. Diagnosis of certain neurological conditions, pernicious anemia, atrophic gastritis, gastric carcinoma, Zollinger-Ellison syndrome. |
| What are some clinical uses of H1 antagonists? | Prevent and relieve the symptoms of allergic rhinoconjunctivitis. Dependent on agent and dose may provide protection against bronchospasm induced by stimuli such as exercise, cold air. Refractory urticaria. |
| What are the major S.E. of first generation H1 antagonists? | CNS effects (somnolence, diminished alertness, slowed reaction time, and impairment of cognitive function). Anticholinergics effects (dry mouth, blurred vision, urinary retention, impotence). Tachycardia, prolongation of Q-T interval, heart block, dysrhythmias. |
| What are the symptoms of OD associated with H1 antagonists? | Coma, seizures, dyskinesias, hallucinations. |
| What are the major S.E. of 2nd generation H1 antagonists? | Unlikely to produce CNS effects unless recommended are exceeded. Prolongation of Q-T interval. |
| How do 1st generation and 2nd generation H1 antagonists differ? | 1st generation tend to produce sedation and may block muscarinic cholinergic, 5-hydroxytrytptomine (serotonin), or alpha adrenergic receptors. At high doses act as competitive antagonists. 2nd generation are more selective therefor have less CNS effects. Act as non-competitive antagonists. |
| What agents are used as H2 antagonists? | Cimetidine, ranitidine, famotidine, nizatidine. |
| What are the clinical uses of H2 antagonists? | Duodenal ulcers associated with hypersecretion of gastric hydrogen ions. Preoperatively used to ↑ the pH of gastric fluid. ↓ risk of acid pneumonitis. Given to patients with history of allergic reactions prior to procedures (dyes). |
| What are the clinical uses of H2 antagonists combined with H1? | Prevent effects of histamine releasing drugs such as morphine, atracurium, mivacurium, or protamine. |
| What is the MOA of H2 antagonists? | Competitively and selectively inhibit the binding of histamine to the H2 receptors. |
| What are the most serious adverse reactions with H2 antagonists? | Severe S.E. with all 4 H2 agents are low but increases in the presence of multiple medical illnesses and advanced age. Reversible increases in hepatic transaminases, esp. with high doses. |
| What are the most common S.E. associated with H2 antagonists? | Diarrhea, HA, fatigue, muscle pain. |
| What are the rare S.E. associated with H2 antagonists? | Mental confusion, dizziness, somnolence, gynecomastia, thrombocytopenia, drug fever, arrhythmias. |
| What S.E. are associated with cimetidine and ranitidine? | Bradycardia. |
| What S.E. occur with rapid administration of H2 antagonists? | Bradycardia and hypotension. |
| What is the principal mechanism of drug interactions associated with cimetidine? | Impairment of hepatic microsomal (cytochrome P-450) enzymes. |
| What are the most common drug interactions associated with the use of cimetidine? | Inhibits metabolism of propranolol, and diazepam. Increases toxicity of lidocaine, modestly decreases defluronation of methoxyflurane, and inhibits oxidative metabolism of halothane. |
| What are the most common drug interactions associated with the use cimetidine and ranitidine? | Can impair renal tubular secretion of procainamide and theophylline. |
| Which agents can decrease the absorption of H2 antagonists? | Magnesium and aluminum containing antacids. |
| How do the H2 antagonists differ in potency and duration? | Potencies vary from 20-50 fold. Cimetidine is least potent, famotidine is most potent. DOA range from 6 hrs with cimetidine to 10 hrs with ranitidine, famotidine, nizatidine. |
| How are H2 antagonists eliminated? | Renal clearance is 2-3 times greater than glomerular filtration reflecting extensive renal tubular secretion. |
| What are proton pump inhibitors? | Drugs that provide prolonged inhibition of gastric acid secretion regardless of stimulus. |
| What are the clinical uses of these agents? | Inhibits daytime and nocturnal acid secretion and meal stimulated acid secretion to a greater degree than H2. Heal duodenal and possibly gastric ulcers faster than H2. Superior to H2 for tx of reflux esophagitis, best tx for Zolliner-Ellison syndrome. |
| What agents are proton pump inhibitors? | Esomeprazole, lansoprazole, omeprazole, pantoprazole. |
| What is cromolyn? | An antihistamine that has poor oral absorption therefore given via inhalation. |
| What is the use of cromolyn? | Prophylactic tx of asthma. |
| What is the MOA of cromolyn? | Inhibits antigen-induced release of histamine and other autocoids, including leukotrienes, from pulmonary mast cells, as well as from mast cells at other sites. |
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