ANSIMAR CLASSIFICATION: Bronchodilator.

MOA: Adrenergic bronchodilators and phosphodiesterase inhibitors bothwork by increasing intracellular level of cyclic-3,5- adenosine monophosphate(cAMP); adrenergics by increasing production and phosphodiesterase inhibitors by decreasing breakdown. Increased levels of cAMP produce bronchodilation.C o r t i c o s t e r o i d s a c t b y d e c r e a s i n g a i r w a y i n f l a m m a t i o n . A n t i c h o l i n e r g i c s (ipratropium) produce bro ndho dilation by decreasing intracellul ar levels of cyclic guanosine monophosphate (cGMP). Leukotriene receptor antagonists andmast cell stabilizers decrease the release of substances that can contribute to bronchospasm. INDICATIONS: Bronchial asthma & pulmonary disease w/ spastic bronchial component. CI: Acute MI, hypotension, lactation. SIDE EFFECTS: Nausea, vomiting, epigastric pain, cephalalgia, irritability, insomnia, tachycardia, extrasystole, tachypnea, hyperglycemia, albuminuria. ADVERSE EFFECTS: NURSING CONSIDERATION: Use with caution in patients with hypoxemia, hyperthyroidism, liver disease, renal disease, in those with history of peptic ulcer and in elderly. Frequently, patients with CHF have markedly prolonged drug serum levels following discontinuation of

Ansimar. > assess for allergic reaction > assess for breath sounds >should be given to a pregnant woman only if clearly needed. Monitor heart rate, CNS stimulation, notify physician if palpitations, chest pain,tachycardia occurs

MACRODANTIN CLASS: antibiotic MOA: Nitrofurantoin interferes with the production of bacterial proteins, DNA, and cell walls. Bacteria cannot survive without a cell wall or multiply without DNA. Nitrofurantoin is reduced by bacterial flavoproteins to reactive intermediates which inactivate or alter bacterial ribosomal proteins and other macromolecules. As a result of such inactivations, the vital biochemical processes of protein synthesis, aerobic energy metabolism, DNA synthesis, RNA synthesis and cell wall synthesis are inhibited. The broad-based nature of this mode of action may explain the lack of acquired bacterial resistance to nitrofurantoin, as the necessary multiple and simultaneous mutations of the target macromolecules would likely be lethal to the bacteria. I: The treatment of urinary tract infections, e.g., cystitis, when due to susceptible strains of E. coli, enterococci, S. aureus and certain susceptible strains of Klebsiella species, Enterobacter species and Proteus species. CI: Anuria, oliguria or significant impairment of renal function (creatinine clearance under 60 mL/min or clinically significant elevated serum creatinine) are contraindications to therapy with this drug. S/E: vomiting, loss of appetite, diarrhea, and abdominal pain.

A/E: Respiratory: Chronic, subacute or acute pulmonary hypersensitivity reactions may occur with the use of nitrofurantoin; Malaise, dyspnea on exertion, cough and altered pulmonary function are common manifestations which can occur insidiously. NSG. RESP: Stomach upset also can be minimized by using a lower dose or by taking nitrofurantoin with food or milk. Antacids containing magnesium trisilicate, when administered concomitantly with nitrofurantoin, reduce both the rate and extent of absorption.

COMBIVENT CLASS: MOA: Ipratropium and albuterol combination reduces bronchospasm through both anticholinergic and sympathomimetic mechanisms. Simultaneous administration of both drugs produces a greater bronchodilator effect than when either drug is used alone at recommended dosages.
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AlbuterolAlbuterol is a sympathomimetic agent that has a relatively high degree

of selectivity for beta 2-adrenergic receptors. Activation of these receptors on airway smooth muscle leads to the activation of the enzyme adenylyl cyclase and to an increase in the intracellular concentration of cyclic-3, 5-adenosine monophosphate (cAMP). Increased cAMP concentrations indirectly lower intracellular ionic calcium, which results in airway smooth muscle relaxation.
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IpratropiumIpratropium is an anticholinergic agent that produces a local, site-specific effect rather than a systemic effect. It appears to produce bronchodilation by inhibition of cholinergic receptors on bronchial smooth muscle.

I: For the management of bronchospasm in patients suffering from chronic obstructive pulmonarydisease (COPD) who requires regular treatment with both ipratropium and salbutamol. CI: Patients with cardiac tachyarrhythmias, hypertrophic obstructive cardiomyopathy and patientswith a history of hypersensitivity to any of its components or to atropine or its derivatives. S/E: Signs of potential side effects, especially chest discomfort or pain, irregular heartbeat, oropharyngeal edema, skin rash, tachycardia, and urticaria A/E: angioedema, paradoxical or hypersensitivity-induced bronchospasm, NSG.RESP: monitor respiratory status; auscultate lungs before and after inhalationreport treatment failure (exacerbation of respiratory symptoms) to physician do not allow the solution/ mist to enter the eyes consult a doctor immediately in the event of acute, rapidly worsening dyspnea. In addition, the patient should be warned to seek medical advice should a reduced response become apparent.

Eye pain or discomfort, blurred vision, visual halos or colored images in association with red eyes from conjunctival and corneal congestion may be signs of acute narrowangle glaucoma. Should any combination of these symptoms develop, treatment with miotic drops should be initiated and specialist advice sought immediately. allow 30-60 sec between puffs for optimum results. wait 5 min between this and other inhaled medications. rinse mouth after medication puffs to reduce bitter taste

MYRIN FORTE CLASS: J04AM06 - rifampicin, pyrazinamide, ethambutol and isoniazid ; Belongs to the class of combination drugs used in the systemic treatment of tuberculosis. MOA: Inhibits RNA synthesis, decreases tubercle bacilli replication (r) Isoniazid is a prodrug and must be activated by a bacterial catalase-peroxidase enzyme that in M. tuberculosis is called KatG.[5] KatG couples the isonicotinic acyl with NADH to form isonicotinic acylNADH complex. This complex binds tightly to the enoyl-acyl carrier protein reductase known as InhA, thereby blocking the natural enoyl-AcpM substrate and the action of fatty acid synthase. This process inhibits the synthesis of mycolic acid, required for the mycobacterial cell wall. (I) Pyrazinamide diffuses into M. tuberculosis, where the enzyme pyrazinamidase converts pyrazinamide to the active form pyrazinoic acid. Under acidic conditions, the pyrazinoic acid that slowly leaks out converts to the protonated conjugate acid, which is thought to diffuse easily back into the bacilli and accumulate. The net effect is that more pyrazinoic acid accumulates inside the bacillus at acid pH than at neutral pH.[6] Pyrazinoic acid was thought to inhibit the enzyme fatty acid synthase (FAS) I, which is required by the bacterium to synthesise fatty acids[7] although this has been discounted.[8] It was also suggested that the accumulation of pyrazinoic acid disrupts membrane potential and interferes with energy production, necessary for survival of M. tuberculosis at an acidic site of infection. (P) Ethambutol is bacteriostatic against actively growing TB bacilli. It works by obstructing the formation of cell wall. Mycolic acids attach to the 5'-hydroxyl groups of D-arabinose residues of arabinogalactan and form mycolyl-arabinogalactan-peptidoglycan complex in the cell wall. It disrupts arabinogalactan synthesis by inhibiting the enzyme arabinosyl transferase. Disruption of the

arabinogalactan synthesis inhibits the formation of this complex and leads to increased permeability of the cell wall. I: Initial phase treatment & re-treatment of all forms of TB in category I & II patients caused by susceptible strains of mycobacteria. CI: Hypersensitivity. Alcoholism, optic neuritis, impaired hepatic function, severe renal insufficiency, hyperuricemia, gouty arthritis, jaundice, retrobulbar neuritis. Patients who are unable to appreciate & report visual side effects or changes in vision eg young childn & patients w/ mental illness or deficiency. Patients <40 kg. Lactation. Pyrazinamide: Severe hepatic damage. Concurrently taking medications associated w/ liver injury, drink excessive amounts of alcohol, underlying liver disease or history of INH-associated liver injury. S/E: dizziness, paresthesia; epigastric distress, constipation, nausea, vomiting, anorexia; hepatic impairment, jaundice; pruritus, rash, acute gout; malaise; headache; mental confusion; A/E: Leukopenia, thrombocytopenia, hypersensitivity syndrome, eosinophilia, fever, lymphadenopathy; anorexia, elevations of serum uric acid conc; NSG.RESP: Should be taken on an empty stomach. (Take 1 hr before or 2 hr after meals. May be taken w/ meals or antacids to reduce GI discomfort. Do not take w/ Al-containing antacids.) An extra patient leaflet is available with Exforge. Talk to your pharmacist if you have questions about this information. Take Exforge by mouth with or without food. Take Exforge on a regular schedule to get the most benefit from it. Taking Exforge at the same time each day will help you remember to take it. If you miss a dose of Exforge, take it as soon as possible. If it is almost time for your next dose, skip the missed dose and go back to your regular dosing schedule. Do not take 2 doses at once.