c. inhalation of aerosolized particlesd. aspiration of oropharyngeal secretions (most common) B.

Etiology Classical community acquired pneumonia is most frequently caused by S. pneumoniae.However, H. influenzae and M. tuberculosis become more frequent in older age groups. Gramnegative bacilli are also sometime responsible for causing pneumonia.Atypical pneumonia is usually caused by M. pneumoniae, C. pneumoniae, and numerous viruses(incl. adenovirus, parainfluenza virus, respiratory syncytial virus).[Table modified from Cecil Essentials of Medicine, 4th ed.] Pathogens Causing Pneumonia According to Population

Population

Pathogens children and younger adultsS. pneumoniae, M. pneumoniae, C. pneumonia, RSVelderly adults S. pneumoniae, influenza virus, M. tubuerculosischronically ill S. pneumoniae, influeza virus, oropharyngeal flora, M.tuberculosis, Gram neg. bacillihospitalized oropharyngeal flora, S. aureus, Gram neg. bacilli, L. pneumophila C. Clinical Features Clinical features of pneumonia vary greatly according to etiologic agent responsible and population affected.Most patients have a cough, fever, increased heart rate, and increased respiration rate. Patientsmay also experience pleuritic pain, hemoptysis, systemic upset, and confusion.Classical community acquired pneumonia presents with abrupt onset of single shaking chill,cough, rust-coloured sputum, and moderate fever.Atypical community acquired pneumonia has a less severe course with more prominent systemicsymptoms and less prominent respiratory symptoms. Patients may only present with tachypnea,dry cough, and mild fever. D. Radiographic Patterns Chest radiographs can rule out the possibility of pneumonia or help differentiate between

bacterial and viral pneumonias. Or, they may point to a diagnosis of presumptive pneumoniawhen the patient presents with only mild symptoms, eg in the elderly.The pattern of the chest radiograph gives clues to the etiology of pneumonia. Lobar consolidation suggests a bacterial pathogen whereas patchy, bilateral infiltrates with little or no pleural effusion are usually seen in atypical pneumonias.Large pleural effusions may point to streptococcal pneumonia or tuberculosis. Cavitationsindicates a necrotizing pneumonia, such as that caused by tuberculosis or S. aureus.It is important to remember that early in the course of acute bacterial pneumonias, the chestradiographs may yield little information as they often appear normal initially. Therefore it isimportant to conduct other laboratory tests, as will be discussed later. E. Diagnosis The use of chest radiographs in diagnosis has already been described in the previous section.Other tests that may narrow the differential diagnosis include WBC count which tend to bemarkedly elevated in bacterial pneumonia.If the patient has a productive cough, it is important to obtain a sputum sample. Empiric therapyfor community acquired pneumonia without obtaining a sputum sample is effective in mostcases. However, this encourages the widespread and indiscriminate use of broadspectrumantibiotics and contributes to increases in antibiotic resistance.A good sputum sample contains no squamous epithelial cells and at least 10-15 PMN per high power field. If the patient is too ill to provide a sputum sample, nasotracheal or transtrachealaspiration may be used.The specimen should be gram stained and examined under oil immersion. This is often enough toidentify the pathogen. The presence of large numbers of PMNs and WBCs also suggests a bacterial agent that is responsible. If only inflammatory cells and few WBC are seen, anonbacterial etiology should be considered.If no clear diagnosis of bacterial pneumonia is fiound, the sample should be stained with an acid-fast stain to indentify mycobacteria. Other less common stains are available to identifylegionnella and fungal pathogens. The sample should be cultured and tested for antibioticresistance. F. Management and Treatment Upon identification of the responsible pathogen, the patient should be immediately givenantibiotic treatment. Penicillin is the drug of choice for pneumococcal pneumonia. Erythromycincan be used if the patient is allergic to penicillin or if the cultures were either inconclusive or demonstrated an atypical pneumonia. Most patients can be treated on an outpatient basis.

Patients who are at risk for developing respiratory failure or who are tachypneic or hypoxemicshould be hospitalized. Their treatment may include some or all of the following:- supplemental oxygenmonitoring in critical care unit- frequent clapping and drainage if patient cannot cough properly-

suctioning of oral secretions- isolation in room with negative pressure if patient has suspected pulmonary TB- analgesia for pleuritic pain- fluid replacement G. Prevention Pneumococcal pneumonia is preventable in 60-80% of patients if they are given a pneumococcalvaccine (23 valent Pneumovax II 0.5 mL sc).This one-time vaccine should be offered to patients suffering from:chronic heart or lung conditions- cirrhosis- chronic renal failure, nephrosis- diabetes mellitusimmunosuppression, HIV infection, Hodgkin's diseae, multiple myeloma- sickle-cell disease- patients > 65 yoYearly influenza vaccine may also be indicated in these patients.

Indication & Dosage

Oral

Prophylaxis in thromboembolic disorders including myocardial infarction, peripheral arterial disease and stroke Adult: 75 mg once daily. CrCl (ml/min) 5-15 Dosage Recommendation

Use with caution.

Hepatic impairment: Severe hepatic impairment: Use with caution. Administration May be taken with or without food. Overdosage Prolonged bleeding time and subsequent bleeding complications. If quick reversal is required, platelet transfusion may be considered. Contraindications Hypersensitivity. Active pathological bleeding. admin within 7 days after MI and ischaemic stroke, coagulation disorders. Lactation. Special Precautions Patients at risk of increased bleeding from trauma, surgery, or other pathological conditions; ulcer; renal and hepatic impairment; history of bleeding or haemostatic disorders. Pregnancy. Adverse Drug Reactions Dyspepsia, abdominal pain, nausea, vomiting, flatulence, constipation, gastritis, gastric and duodenal ulcers. GI upset, diarrhoea, paraesthesia, vertigo, headache, dizziness, pruritus and rashes. Potentially Fatal: Bleeding disorders including GI and intracranial haemorrhage. Blood dyscrasias. Drug Interactions Co-admin with NSAIDs may increase the risk of stomach and intestinal bleeding. High-dose clopidogrel may lead to increased warfarin levels thus increasing the risk of bleeding. High-

dose clopidogrel may also inhibit P450 (2C9), thus interfering with the metabolism of phenytoin, tamoxifen, torasemide, fluvastatin and some NSAIDs. Click to view more clopidogrel Drug Interactions Pregnancy Category (US FDA)

Category B: Either animal-reproduction studies have not demonstrated a foetal risk but there are no controlled studies in pregnant women or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the 1st trimester (and there is no evidence of a risk in later trimesters). Storage Oral: Store at 25C. Mechanism of Action Clopidogrel inhibits adenosine diphosphate (ADP) from binding to its receptor sites on the platelets and subsequent activation of glycoprotein GP IIb/IIIa complex thus preventing fibrinogen binding, platelet adhesion and aggregation. Absorption: Rapidly but incompletely absorbed from the GI tract (oral). Distribution: Protein-binding: Extensive. Metabolism: Hepatic: Extensive; converted to inactive carboxylic acid derivative and thiol derivative (active). Excretion: Via urine and faeces (as metabolites and unchanged drug). MIMS Class Anticoagulants, Antiplatelets & Fibrinolytics (Thrombolytics)

ATC Classification B01AC04 - Clopidogrel ; Belongs to the class of platelet aggregation inhibitors excluding heparin. Used in the treatment of thrombosis.