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NURS615 Updated PHarm 4 test review notes NURS615 Updated PHarm 4 test review notes NURS615 Updated PHarm 4 test review notes
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1. What is tiotropium used to treat? Tiotropium bromide (originally marketed as Spiriva ) is a long-acting, 24-hour, anticholinergic bronchodilator used in the management of chronic obstructive pulmonary disease (COPD).Tiotropium is used for maintenance treatment of chronic obstructive pulmonary disease (COPD) which includes chronic bronchitis and emphysema.[4]^ It is not however used for acute exacerbations. Adverse effects Adverse effects are mainly related to its antimuscarinic effects. Common adverse drug reactions (≥1% of patients) associated with tiotropium therapy include: dry mouth and/or throat irritation. Rarely (<0.1% of patients) treatment is associated with :urinary retention, constipation, acute angle closure glaucoma, palpitations (notably supraventricular tachycardia and atrial fibrillation) and/or allergy (rash, angioedema, anaphylaxis). Tiotropium and another member of its class ipratropium were linked to increased risk of heart attacks, stroke and cardiovascular death.[6]^ Tiotropium mist inhaler (Respimat) has been found to be associated with an increase of all cause mortality in people with COPD. Dosage: The standard dose of tiotropium is 18 mcg which is administered by a HandiHaler inhalation device.[9] Mechanism of action: Tiotropium is a muscarinic receptor antagonist, often referred to as an antimuscarinic or anticholinergic agent. Although it does not display selectivity for specific muscarinic receptors, when topically applied it acts mainly on M 3 muscarinic receptors located on smooth muscle cells and submucosal glands. This leads to a reduction in smooth muscle contraction and mucus secretion and thus produces a bronchodilatory effect. 2. What are the adverse effects with Montelukast (Singular)? Montelukast (trade name Singulair ) is a leukotriene receptor antagonist (LTRA) used for the maintenance treatment of asthma and to relieve symptoms of seasonal allergies. Montelukast comes as a tablet, a chewable tablet, flash tablet and granules to take by mouth. Montelukast is usually taken once a day with or without food. Montelukast is a CysLT 1 antagonist; it blocks the action of leukotriene D4 (and secondary ligands LTC4 and LTE4) on the cysteinyl leukotriene receptor CysLT 1 in the lungs and bronchial tubes by binding to it. This reduces the bronchoconstriction otherwise caused by the leukotriene and results in less inflammation. Because of its mechanism of action, it is not useful in the treatment of acute asthma attacks. The Mont in Montelukast stands for Montreal, the place where Merck developed the drug. Medical Uses: Montelukast is used for a number of conditions including asthma, exercise induced bronchospasm, allergic rhinitis, primary dysmenorrhoea (i.e. dysmenorrhoea not associated with known causes; see dysmenorrhea causes), and urticaria. It is mainly used as a complementary therapy in adults in addition to inhaled corticosteroids, if they alone do not bring the desired effect. It is also used to prevent allergic reactions and asthma flare-ups during the administration of intravenous immunoglobulin.
Montelukast is administered as montelukast sodium, with 5.2 mg of montelukast sodium being equivalent to 5 mg of montelukast.
6. What is the mechanism of action of Albuterol? This is a relatively selective β 2 - adrenergic bronchodilator used for relief of bronchospasm in patients with reversible obstructive airway disease. Called also salbutamol. The pharmacologic effects of beta-adrenergic agonist drugs, including Albuterol, are at least in part attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'- adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. They act on the smooth muscles within the bronchial tree. Patient Teaching: Store albuterol in a cool, dry place out of light. Take the medicine as directed. If you take albuterol as a rescue medicine, keep it with you at all times. If you need to take more medicine to help with breathing than has been prescribed, contact your health care provider. A different medicine may be needed. Tell your doctor or health care provider if you have any of these conditions. There may be reasons to not use albuterol medicines: Heart disease or high blood pressure Allergy to albuterol, levalbuterol, sulfites, preservatives or dyes. Your health care provider may talk with you about other medicines for breathing. History of seizures Diabetes. Albuterol can raise blood glucose levels. Side Effects Some of the common side effects of albuterol are: Feel nervous or shaky Cough or sore throat Headache Runny or stuffy nose Dry mouth or throat Sleeping problems
Most potent and effective anti-inflammatory medication currently available. Lead to reduction in severity of asthma symptoms. Increase peak flow readings. Decrease airway hyperresponsiveness. Safe and tolerated at recommended dosages and can be used for both children and adults. Commonly prescribed inhaled corticosteroid used is beclomethasone dipropionate (QVAR), triamcinolone acetonide (Azmacort), budesomide (Pulmicort), flunisolide (AeroBid), mometasone furoate (Asmanex Twsthaler), fluticasone (Flovent), and ciclesonide (Alvesco).
Dose in adults is 60mg q 4 - 6 hours, dose in children age 6 - 12 years is 30mg every 4 - 6 hours.
➢ Aluminum and Calcium based antacids cause constipation ➢ Magnesium based antacids cause diarrhea
inhibitors (PPIs)?
41. Loop diuretics — When administered at maximum dose, the loop diuretics, furosemide, bumetanide, torsemide, and ethacrynic acid, can lead to the excretion of up to 20 to 25 percent of filtered sodium [1,10]. They act in the medullary and cortical aspects of the thick ascending limb, including the macula densa cells in the early distal tubule. At each of these sites, sodium entry is primarily mediated by a Na-K-2Cl carrier in the luminal membrane that is activated when all four sites are occupied (figure 2) [1,5,11,12]. The loop diuretics appear to compete for the chloride site on this carrier, thereby diminishing net reabsorption [12,13]. Inhibition of an isoform of this cotransporter in the inner ear is thought to be responsible for the ototoxicity that is rarely seen with high dose intravenous loop diuretic therapy. (See "Treatment of refractory edema in adults", section on 'Risk of ototoxicity'.)
Loop diuretics also have important effects on renal calcium handling. The reabsorption of calcium in the loop of Henle is primarily passive, being driven by the electrochemical gradient created by NaCl transport and occurring through the paracellular pathway [14,15]. As a result, inhibiting the reabsorption of NaCl leads to a parallel reduction in that of calcium, thereby increasing calcium excretion. In the past, saline plus high doses of furosemide was a mainstay of the treatment of hypercalcemia. Volume expansion is still important, but other drugs, such as bisphosphonates, have largely replaced loop diuretics in this setting. (See "Treatment of hypercalcemia".)