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Toxin Induced pulmonary edema

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1. Toxin Induced pulmonary edema

Toxin Induced pulmonary edema Toxin Induced pulmonary edema Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Toxin Induced pulmonary (...) edema Toxin Induced pulmonary edema Aka: Toxin Induced pulmonary edema II. Causes (Mnemonic: MOPS) , s Phenobarbital, Propoxyphene s Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Toxin Induced pulmonary edema." Click on the image (or right click) to open the source website in a new browser window. Related Studies (from Trip Database) Related Topics in Radiology About FPnotebook.com is a rapid access, point-of-care medical

2018 FP Notebook

2. Hsp70 Suppresses Mitochondrial Reactive Oxygen Species and Preserves Pulmonary Microvascular Barrier Integrity Following Exposure to Bacterial Toxins (PubMed)

unacceptably high in part due to the release of bacterial toxins. Pneumolysin (PLY) is a cholesterol-dependent toxin that is produced by Streptococcus, and it is both necessary and sufficient for the development of the extensive pulmonary permeability edema that underlies acute lung injury. The mechanisms by which PLY disrupts the pulmonary endothelial barrier are not fully understood. Previously, we found that reactive oxygen species (ROS) contribute to the barrier destructive effects of PLY (...) Hsp70 Suppresses Mitochondrial Reactive Oxygen Species and Preserves Pulmonary Microvascular Barrier Integrity Following Exposure to Bacterial Toxins Pneumonia is a leading cause of death in children and the elderly worldwide, accounting for 15% of all deaths of children under 5 years old. Streptococcus pneumoniae is a common and aggressive cause of pneumonia and can also contribute to meningitis and sepsis. Despite the widespread use of antibiotics, mortality rates for pneumonia remain

Full Text available with Trip Pro

2018 Frontiers in immunology

3. CRACKCast E159 – Inhaled Toxins

(asbestos). Therapy targets clinical manifestations of the inhaled toxins. See [Table 153-1] for a long list of common inhaled toxins. They can fall into different classifications: Irritants Simple asphyxiants Chemical asphyxiants (carbon monoxide; hydrogen cyanide; phosphine) 5 recognized categories: Simple asphyxiants (CO2; methane; nitrogen gas; nitrous oxide; noble gases) Displace oxygen Pulmonary irritants (e.g pharmacologic CS or chloroacetophenone gas – tear gas; ammonia; phosgene ozone) Direct (...) pulmonary irritation Smoke/soot Inhalation Irritation & O2 displacement Cyanide & Hydrogen Sulfide Cellular toxicity Inhibits oxidative phosphorylation Carbon Monoxide hypoxia All these agents have varying solubility and some may have profound systemic effects (hydrofluoric acid for example: very irritating, highly soluble and profound systemic effects). Toxic Progression goes a little something like this: Airway edema Bronchoconstriction Pneumonitis ARDS Resp Failure Death OR Inhalation of cellular

2018 CandiEM

4. Toxin Induced pulmonary edema

Toxin Induced pulmonary edema Toxin Induced pulmonary edema Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Toxin Induced pulmonary (...) edema Toxin Induced pulmonary edema Aka: Toxin Induced pulmonary edema II. Causes (Mnemonic: MOPS) , s Phenobarbital, Propoxyphene s Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Toxin Induced pulmonary edema." Click on the image (or right click) to open the source website in a new browser window. Related Studies (from Trip Database) Related Topics in Radiology About FPnotebook.com is a rapid access, point-of-care medical

2015 FP Notebook

5. Toxin Induced Vital Sign Changes

Hypnotics (e.g. s) (and s) VII. Causes: Hypertension (Mnemonic=CTSCAN) See Supplements s s, s Nicotine VIII. Causes: Hypoventilation (Mnemonic=SLOW) Sedative hypnotics Liquor ( ) s Weed ( ) IX. Causes: Hyperventilation (Mnemonic=PANT) (PCP) or Pneumonitis (Chemical) ( s) Non-cardiogenic pulmonary edema Toxic Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Toxin Induced Vital Sign Changes." Click on the image (or right click) to open (...) Toxin Induced Vital Sign Changes Toxin Induced Vital Sign Changes Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Toxin Induced Vital

2018 FP Notebook

6. Diagnosis of chronic thromboembolic pulmonary hypertension: A Canadian Thoracic Society clinical practice guideline update

thromboembolic material? In patients with suspected CTEPH, should magnetic resonance pulmonary angiography (MRPA) be used to establish the diagnosis and assess the anatomic extent and location of chronic thromboembolic material? Table 1. Updated clinical classification of pulmonary hypertension (PH). 2 1. PAH 1.1 Idiopathic PAH 1.2 Heritable PAH 1.3 Drug – and toxin-induced PAH 1.4 PAH associated with: 1.4.1 Connective tissue disease 1.4.2 HIV infection 1.4.3 Portal hypertension 1.4.4 Congenital heart (...) Diagnosis of chronic thromboembolic pulmonary hypertension: A Canadian Thoracic Society clinical practice guideline update CTS GUIDELINES AND POSITION PAPERS Diagnosis of chronic thromboembolic pulmonary hypertension: A Canadian Thoracic Society clinical practice guideline update Doug Helmersen a , Steeve Provencher b , Andrew M. Hirsch c , Anne Van Dam d , Carole Dennie e , Marc De Perrot f , Lisa Mielniczuk g , Naushad Hirani a , George Chandy h , John Swiston i , Dale Lien j , Nick H. Kim k

2019 Canadian Thoracic Society

7. Pulmonary Edema, Cardiogenic (Overview)

Pulmonary Edema, Cardiogenic (Overview) Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTU3NDUyLW92ZXJ2aWV3 processing > Cardiogenic Pulmonary Edema (...) Updated: Dec 21, 2017 Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Henry H Ooi, MD, MRCPI Share Email Print Feedback Close Sections Sections Cardiogenic Pulmonary Edema Overview Background Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects the accumulation of fluid with a low-protein content in the lung interstitium and alveoli as a result of cardiac dysfunction (see

2014 eMedicine.com

8. Pulmonary Edema, Cardiogenic (Diagnosis)

Pulmonary Edema, Cardiogenic (Diagnosis) Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTU3NDUyLW92ZXJ2aWV3 processing > Cardiogenic Pulmonary Edema (...) Updated: Dec 21, 2017 Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Henry H Ooi, MD, MRCPI Share Email Print Feedback Close Sections Sections Cardiogenic Pulmonary Edema Overview Background Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects the accumulation of fluid with a low-protein content in the lung interstitium and alveoli as a result of cardiac dysfunction (see

2014 eMedicine.com

9. Suspected Pulmonary Hypertension

(PVOD) and/or pulmonary capillary hemangiomatosis (PCH); Group 1 ?, persistent PH of the newborn; Group 2, PH due to left heart disease; Group 3, PH due to lung diseases and/or hypoxia; Group 4, CTEPH and other pulmonary artery obstructions; and Group 5, PH with unclear and/or multifactorial mechanisms [2] (see Appendix 1). The signs and symptoms of PH are nonspecific and may include fatigue, dyspnea, weakness, angina, peripheral edema, hepatomegaly, ascites, and syncope [10,11]. Because (...) of the nonspecific symptoms as well as the large, diverse group of diseases that can cause PH, diagnosis can be challenging. A careful history is critical to evaluate for risk factors for PH, including family history, history of drugs and toxins associated with PH, collagen vascular disease, human immunodeficiency virus (HIV), portal hypertension, congenital or left heart disease, and venous thromboembolic disease [11,12]. Clinical evaluation includes pulmonary function tests, arterial blood gases, routine

2016 American College of Radiology

10. Pediatric Pulmonary Hypertension

disease. 200,201 However, surfactant did not reduce ECMO use in newborns with idiopathic PPHN and carries a risk for acute airway obstruction. 201 Therefore, the use of surfactant should be considered only for infants with severe parenchymal lung disease and poor lung recruitment. In some cases, lung recruitment may be sufficient to lower PVR without the need for PH-specific therapy or may enhance responsiveness to iNO. 202 Acidosis can induce pulmonary vasoconstriction and should be avoided. Forced (...) Neurofibromatosis Autoimmune polyendocrine syndrome Gaucher disease Glycogen storage disease I and III Mitochondrial disorders (MELAS) CHD indicates congenital heart disease; MELAS, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes; PH, pulmonary hypertension; and SCD, sickle cell disease. Downloaded from http://ahajournals.org by on March 27, 2019Abman et al Pediatric Pulmonary Hypertension 2057 paradoxically worsen pulmonary vascular tone, reactivity, and permeability edema 203

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2015 American Heart Association

11. Pediatric Pulmonary Hypertension: ATS/AHA Clinical Practice Guidelines

obstruction. 201 Therefore, the use of surfactant should be considered only for infants with severe parenchymal lung disease and poor lung recruitment. In some cases, lung recruitment may be sufficient to lower PVR without the need for PH-specific therapy or may enhance responsiveness to iNO. 202 Acidosis can induce pulmonary vasoconstriction and should be avoided. Forced alkalosis induced by hyperventila- tion or infusion of sodium bicarbonate was frequently used before the approval of iNO. 185 Although (...) ) CHD indicates congenital heart disease; MELAS, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes; PH, pulmonary hypertension; and SCD, sickle cell disease. by guest on March 15, 2016 http://circ.ahajournals.org/ Downloaded from Abman et al Pediatric Pulmonary Hypertension 21 paradoxically worsen pulmonary vascular tone, reactivity, and permeability edema 203 and may produce cerebral constriction, reduced cerebral blood flow, and worse neurodevelopmental outcomes

2015 American Thoracic Society

12. Pharmacologic Therapy for Pulmonary Arterial Hypertension in Adults

Pharmacologic Therapy for Pulmonary Arterial Hypertension in Adults 449 journal.publications.chestnet.org Pha r maco logic Th erapy for Pulmonary Arterial Hypertension in Adults CHEST Guideline and Expert Panel Report Darren B. Taichman , MD, PhD, FCCP ; Joe Ornelas , MS ; Lorinda Chung , MD ; James R. Klinger , MD, FCCP ; Sandra Lewis , PhD ; Jess Mandel , MD ; Harold I. Palevsky , MD, FCCP ; Stuart Rich , MD, FCCP ; Namita Sood , MD, FCCP ; Erika B. Rosenzweig , MD ; Terence K. Trow , MD (...) , FCCP ; Rex Yung , MD, FCCP ; C. Gregory Elliott , MD, FCCP ; and David B. Badesch , MD, FCCP OBJECTIVE: Choices of pharmacologic therapies for pulmonary arterial hypertension (PAH) are ideally guided by high-level evidence. Th e objective of this guideline is to provide clinicians advice regarding pharmacologic therapy for adult patients with PAH as informed by available evidence. METHODS: Th is guideline was based on systematic reviews of English language evidence pub- lished between 1990

2014 American College of Chest Physicians

13. Translational Medicine in Pulmonary-Renal Crosstalk: Therapeutic Targeting of p-Cresyl Sulfate Triggered Nonspecific ROS and Chemoattractants in Dyspneic Patients with Uremic Lung Injury (PubMed)

Translational Medicine in Pulmonary-Renal Crosstalk: Therapeutic Targeting of p-Cresyl Sulfate Triggered Nonspecific ROS and Chemoattractants in Dyspneic Patients with Uremic Lung Injury Molecular mechanisms and pathological features of p-Cresyl sulfate (PCS)-induced uremic lung injury (ULI) in chronic kidney disease (CKD) remain unclear. We analyzed pleural effusions (PE) from CKD and non-CKD patients for uremic toxins, reactive oxygen species (ROS), and chemotactic cytokines. Correlations (...) between PE biomarkers and serum creatinine were also studied. Cell viability and inflammatory signaling pathways were investigated in PCS-treated human alveolar cell model. To mimic human diseases, CKD-ULI mouse model was developed with quantitative comparison of immunostaining and morphometric approach. PE from CKD patients enhance expressions of uremic toxins, hydroxyl radicals, and IL-5/IL-6/IL-8/IL-10/IL-13/ENA-78/GRO α/MDC/thrombopoietin/VEGF. PE concentrations of ENA-78/VEGF/IL-8/MDC/PCS/indoxyl

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2018 Journal of clinical medicine

14. Drug-Induced Pulmonary Toxicity (Diagnosis)

of noncardiac pulmonary edema (NCPE), wheezes in the case of bronchospasm, and decreased breath sounds in pleural effusion. See for more detail. Diagnosis The diagnosis of drug-mediated pulmonary toxicity is usually established based on clinical findings. In general, laboratory analyses are not helpful. Radiologic patterns observed in drug-induced pulmonary toxicity are highly variable and depend on the type of adverse reaction the patient is experiencing. Most drug-induced pulmonary toxicities involve (...) disturb oxidant/antioxidant system homeostasis, resulting in pulmonary injury. Pulmonary vascular damage Drug-induced pulmonary vascular disease manifests clinically as acute pulmonary edema, diffuse interstitial lung disease, pulmonary vascular occlusion, and pulmonary hypertension or hemorrhage. The proposed mechanisms of lung vascular damage include the following: Increased microvascular hydrostatic pressure Increased permeability of the vascular endothelium Vascular occlusion by direct activation

2014 eMedicine.com

15. Drug-Induced Pulmonary Toxicity (Overview)

of noncardiac pulmonary edema (NCPE), wheezes in the case of bronchospasm, and decreased breath sounds in pleural effusion. See for more detail. Diagnosis The diagnosis of drug-mediated pulmonary toxicity is usually established based on clinical findings. In general, laboratory analyses are not helpful. Radiologic patterns observed in drug-induced pulmonary toxicity are highly variable and depend on the type of adverse reaction the patient is experiencing. Most drug-induced pulmonary toxicities involve (...) disturb oxidant/antioxidant system homeostasis, resulting in pulmonary injury. Pulmonary vascular damage Drug-induced pulmonary vascular disease manifests clinically as acute pulmonary edema, diffuse interstitial lung disease, pulmonary vascular occlusion, and pulmonary hypertension or hemorrhage. The proposed mechanisms of lung vascular damage include the following: Increased microvascular hydrostatic pressure Increased permeability of the vascular endothelium Vascular occlusion by direct activation

2014 eMedicine.com

16. Toxin Induced Vital Sign Changes

Hypnotics (e.g. s) (and s) VII. Causes: Hypertension (Mnemonic=CTSCAN) See Supplements s s, s Nicotine VIII. Causes: Hypoventilation (Mnemonic=SLOW) Sedative hypnotics Liquor ( ) s Weed ( ) IX. Causes: Hyperventilation (Mnemonic=PANT) (PCP) or Pneumonitis (Chemical) ( s) Non-cardiogenic pulmonary edema Toxic Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Toxin Induced Vital Sign Changes." Click on the image (or right click) to open (...) Toxin Induced Vital Sign Changes Toxin Induced Vital Sign Changes Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Toxin Induced Vital

2015 FP Notebook

17. Management of Pulmonary Arterial Hypertension

5.4. Others: tumoral obstruction, fibrosing mediastinitis, chronic renal failure on dialysis 1. Pulmonary arterial hypertension (PAH) 1.1. Idiopathic PAH 1.2. Heritable 1.2.1. BMPR2 1.2.2. Activin receptor-like kinase 1(ALK-1), endoglin (with or without hereditary haemorrhagic telangiectasia) 1.2.3. Unknown 1.3. Drug- and toxin-induced 1.4. Associated with: 1.4.1. Connective tissue disease 1.4.2. HIV infection 1.4.3. Portal hypertension 1.4.4. Congenital heart diseases 1.4.5. Schistosomiasis 1.4.6 (...) Pulmonary hypertension owing to lung diseases and/or hypoxia Family history of PAH Heritable PAH Congenital heart diseases Operated and un-operated PAH associated with congenital heart diseases Drug history Psychotropics and appetite suppressants (aminorex, fenfluramine, amphetamines, cocaine etc) Drug and toxin-induced PAH Underlying medical illnesses Connective tissue diseases, HIV infection, haemoglobinopathies, portal hypertension, thyroid diseases, glycogen storage disease, myeloproliferative

2011 Ministry of Health, Malaysia

18. Guidelines on Diagnosis and Treatment of Pulmonary Hypertension

clinical classi?cation of pulmonary hypertension (Dana Point, 2008 1 ) 1 Pulmonary arterial hypertension (PAH) 1.1 Idiopathic 1.2 Heritable 1.2.1 BMPR2 1.2.2 ALK1, endoglin (with or without hereditary haemorrhagic telangiectasia) 1.2.3 Unknown 1.3 Drugs and toxins induced 1.4 Associated with (APAH) 1.4.1 Connective tissue diseases 1.4.2 HIV infection 1.4.3 Portal hypertension 1.4.4 Congenital heart disease 1.4.5 Schistosomiasis 1.4.6 Chronic haemolytic anaemia 1.5 Persistent pulmonary hypertension (...) ), and PAP, 8 the three main parameters of RV pump function. The inadequate adaptation of myocardial Table8 Updated risk level of drugs and toxins known to induce PAH PAH¼ pulmonary arterial hypertension. ESC Guidelines 2501 Downloaded from https://academic.oup.com/eurheartj/article-abstract/30/20/2493/426803 by guest on 02 April 2019contractility seems to be one of the primary events in the pro- gression of heart failure in a chronically overloaded RV. Changes in the adrenergic pathways of RV myocytes

2009 European Society of Cardiology

19. Pulmonary Hypertension, High Altitude (Follow-up)

shows evidence of right ventricular (RV) hypertrophy or strain. After the episode resolves, evidence of RV hypertrophy may or may not persist. The edema fluid is protein-rich, but the primary problem is a hydrostatically induced permeability leak with mild alveolar hemorrhage, which is followed by inflammation. Cardiac catheterization during the acute phase of HAPE reveals pulmonary hypertension with normal wedge or left atrial pressures but increased capillary pressure. This finding supports (...) at moderate altitudes (2,000-3,000 m [approximately 6,500-9,800 ft]). Although this is an uncommon defect, the risk of HAPE in these individuals seems to be extremely high. Overperfusion edema during uneven vasoconstriction induced by high-altitude hypoxia has been suggested as a possible underlying cause. In addition to focusing on genetic susceptibility, speculation concerning the genesis of HAPE has centered on the role of alveolar hypoxia and overperfusion caused by an uneven hypoxic pulmonary

2014 eMedicine Pediatrics

20. Pulmonary Hypertension, Primary (Overview)

represents pulmonary vascular disease with a spectrum of clinical presentations. A complete classification of all pulmonary hypertension (PH) types has been updated [ ] : 1. Pulmonary arterial hypertension (PAH) 1.1 Idiopathic PAH 1.2 Heritable PAH 1.2.1 BMPR2 1.2.2 ALK-1, ENG, SMAD9, CAV1, KCNK3 1.2.3 Unknown 1.3 Drug- and toxin-induced 1.4 Associated with: 1.4.1 Connective tissue disease 1.4.2 HIV infection 1.4.3 Portal hypertension 1.4.4 Congenital heart disease 1.4.5 Schistosomiasis 1'. Pulmonary (...) peptide as a prognostic parameter in patients with pulmonary hypertension. Chest . 2006 May. 129(5):1313-21. . Tolle JJ, Waxman AB, Van Horn TL, Pappagianopoulos PP, Systrom DM. Exercise-induced pulmonary arterial hypertension. Circulation . 2008 Nov 18. 118(21):2183-9. . . Torbicki A, Kurzyna M, Kuca P, Fijalkowska A, Sikora J, Florczyk M, et al. Detectable serum cardiac troponin T as a marker of poor prognosis among patients with chronic precapillary pulmonary hypertension. Circulation . 2003 Aug 19

2014 eMedicine.com

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