Directly from the ACCP Pulmonary medication Board overview 2009 direction, this article covers each subject in a concise, easy-to-use structure. Use as a self-study source to organize for the pulmonary drugs subspecialty board exam.
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Mabeza GF, Macfarlane J. Pulmonary actinomycosis. Eur Resp J 2003; 21:545–551 Comprehensive clinical review of the pulmonary manifestations of actinomycosis. Martinez R, Reyes S, Menendez R. Pulmonary nocardiosis: risk factors, clinical features, diagnosis and prognosis. Curr Opin Pulm Med 2008; 14:219–227 17 Most current, comprehensive clinical review of pulmonary nocardiosis (including expanded sections on newer diagnostic techniques and new therapeutic options). McGeinness G, Naidich DP. CT of airways disease and bronchiectasis.
IPAH is an uncommon disorder affecting women more commonly than men during the ages 20 to 40 years. In approximately 6% of patients, there is a family history of PAH (ie, FPAH), which has been found to be related to 1 of Ͼ 70 identified mutations in the gene-encoding bone morphogenetic protein receptor type II (BMPR2), which is localized to chromosome 2q33. Sporadic mutations in this gene are seen in up to 25% of patients with IPAH. Asymptomatic carriers 28 Table 4. Revised Nomenclature and Classification of PH (2003) from the Third-World Conference on Pulmonary Hypertension* WHO group I PAH IPAH FPAH Associated with Collagen vascular disease Congenital systemic to pulmonary shunts (large, small, repaired, or nonrepaired) Portal hypertension HIV infection drugs and toxins Other (glycogen storage disease, Gaucher disease, hereditary hemorrhagic telangiectasia, hemoglobinopathies, myeloproliferative disorders, splenectomy) Associated with significant venous or capillary involvement Pulmonary venoocclusive disease Pulmonary capillary hemangiomatosis WHO group II Pulmonary venous hypertension Left-sided atrial or ventricular heart disease Left-sided valvular heart disease WHO group III Pulmonary hypertension associated with hypoxemia COPD Interstitial lung disease Sleep-disordered breathing Alveolar hypoventilation disorders Chronic exposure to high altitude WHO group IV PH caused by chronic thrombotic and/or embolic disease Thromboembolic obstruction of proximal pulmonary arteries Thromboembolic obstruction of distal pulmonary arteries Pulmonary embolism (tumor, parasites, foreign material) WHO group V Miscellaneous Sarcoidosis, histiocytosis X, lymphangiomatosis, compression of pulmonary vessels (adenopathy, tumor, fibrosing mediastinitis) *Adapted from Rubin LJ.
Congenital or hereditary hypercoagulable states include the following: activated protein C resistance (factor V Leiden mutation); antithrombin III deficiency (can also be acquired with the nephrotic syndrome); protein C deficiency; protein S deficiency; dysfibrinogenemia; disorders of plasminogen and plasminogen activation; the presence of antiphospholipid antibodies and lupus anticoagulant; and hyperhomocysteinemia. Many patients may present with multiple risk factors for VTE that can further increase their likelihood of this complication developing.
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