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

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

diarrhea. Enterobacter species and Proteus species. . coli. DNA synthesis. CI: Anuria. as the necessary multiple and simultaneous mutations of the target macromolecules would likely be lethal to the bacteria.. the vital biochemical processes of protein synthesis. 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.g. enterococci. and cell walls. and abdominal pain. The broad-based nature of this mode of action may explain the lack of acquired bacterial resistance to nitrofurantoin. aerobic energy metabolism. DNA. S. I: The treatment of urinary tract infections. As a result of such inactivations. RNA synthesis and cell wall synthesis are inhibited. loss of appetite.MACRODANTIN CLASS: antibiotic MOA: Nitrofurantoin interferes with the production of bacterial proteins. aureus and certain susceptible strains of Klebsiella species. e. cystitis. 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. when due to susceptible strains of E.

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

{01} Albuterol—Albuterol is a sympathomimetic agent that has a relatively high degree of selectivity for beta 2-adrenergic receptors. site-specific effect rather than a systemic effect.COMBIVENT CLASS: MOA: Ipratropium and albuterol combination reduces bronchospasm through both anticholinergic and sympathomimetic mechanisms. which results in airway smooth muscle relaxation. It appears to produce bronchodilation by inhibition of cholinergic receptors on bronchial smooth muscle. 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. {01} Ipratropium—Ipratropium is an anticholinergic agent that produces a local. Simultaneous administration of both drugs produces a greater bronchodilator effect than when either drug is used alone at recommended dosages. Increased cAMP concentrations indirectly lower intracellular ionic calcium. . 5-adenosine monophosphate (cAMP).

oropharyngeal edema. especially chest discomfort or pain. In addition. rapidly worsening dyspnea. and urticaria A/E: angioedema. tachycardia. NSG. .RESP:    monitor respiratory status. the patient should be warned to seek medical advice should a reduced response become apparent. 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. irregular heartbeat. S/E: Signs of potential side effects. skin rash.I: For the management of bronchospasm in patients suffering from chronic obstructive pulmonarydisease (COPD) who requires regular treatment with both ipratropium and salbutamol. hypertrophic obstructive cardiomyopathy and patientswith a history of hypersensitivity to any of its components or to atropine or its derivatives. paradoxical or hypersensitivity-induced bronchospasm. CI: Patients with cardiac tachyarrhythmias.

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

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

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

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