HIGH ALTITUDE PULMONORY EDEMA (HAPE)[2305843009213699724].pptx
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High altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes above 2,500 meters. Risk factors include a rapid rate of ascent, a history of HAPE, respiratory infections, cold conditions, and certain cardiopulmonary abnormalities. The pathophysiology involves patchy pulmonary hypoxic vasoconstriction leading to overperfusion in some lung areas and increased capillary pressure, causing fluid to accumulate in the alveoli. Exercise and cold can also increase pulmonary pressures and contribute to HAPE. Prompt descent is needed to treat HAPE, as it remains a major cause of high-altitude related death.
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Chest pain is a common reason for emergency department visits, affecting around 6-7 million people annually in the US. It can be caused by cardiac, pulmonary, gastrointestinal, musculoskeletal, and psychological factors. The initial evaluation of chest pain involves considering the patient's history, symptoms, risk factors, physical exam, ECG, and cardiac biomarkers to determine the likelihood of life-threatening conditions like acute coronary syndrome and pulmonary embolism and guide further testing and treatment. Integrative decision aids are used to assess the probability of acute cardiac events to inform diagnostic and management decisions.
JAUNDICE.pptx
Jaundice is caused by increased levels of bilirubin in the blood which deposits in tissues, causing a yellowish discoloration. It is detected by examining the sclerae. Jaundice can be unconjugated resulting from increased bilirubin production or impaired liver function, or conjugated due to obstruction of the bile ducts. Evaluation of a patient with jaundice includes history, physical exam, liver function tests, and imaging to determine if the cause is hepatocellular injury or obstruction. Treatment depends on identifying and addressing the underlying etiology such as viral hepatitis, gallstones, or cancer.
17.ARDS.ppt
1. Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels in blood, and diffuse lung inflammation and fluid buildup leading to respiratory failure.
2. ARDS has many underlying causes and results from diffuse lung injury. While research has studied many potential treatments, ARDS remains untreatable and mortality remains high.
3. Ventilator management to prevent lung injury without compromising oxygen levels is the main supportive treatment for ARDS.
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Multiple myeloma is a malignant proliferation of plasma cells derived from a single clone. It commonly presents with bone pain, infection, anemia, and renal failure. Diagnosis requires clonal plasma cells ≥10% on bone marrow biopsy along with one or more myeloma defining events including hypercalcemia, renal insufficiency, anemia, or bone lesions. Treatment involves induction therapy such as lenalidomide, bortezomib, and dexamethasone prior to stem cell transplantation for eligible patients, followed by maintenance therapy to improve outcomes. Response is evaluated by monitoring the monoclonal protein and considering additional treatment for relapsed or refractory disease.
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HIGH ALTITUDE PULMONORY EDEMA (HAPE)[2305843009213699724].pptx
- 1. HIGH ALTITUDE PULMONORY EDEMA (HAPE)
- 2. LEARNING OBJECTIVES •High altitude pulmonary edema (HAPE) Risk factors Pathophysiology
- 3. High Altitude Pulmonary Edema(HAPE) • High-altitude pulmonary edema (HAPE) is a life-threatening form of non- cardiogenic pulmonary edema. • Occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). • Cases have also been reported between 1,500–2,500 meters or 4,900–8,200 feet in more vulnerable subjects. • Classically, HAPE occurs in persons normally living at low altitude who travel to an altitude above 2,500 meters (8,200 feet). • Re-entry HAPE is also an entity that has been described in persons who normally live at high altitude but who develop pulmonary edema after returning from a stay at low altitude. It is severe presentation of altitude sickness. • HAPE remains the major cause of death related to high-altitude.
- 4. Risk factors • Rapid rate of ascent • A history of HAPE • Respiratory tract infections • Excessively cold environmental conditions • Men are more susceptible than women • People with abnormalities of the cardiopulmonary circulation leading to pulmonary hypertension. For e.g. Mitral stenosis, Primary pulmonary hypertension. • Patent foramen ovale has also been shown to increase the risk of HAPE
- 5. Pathophysiology • HAPE is characterized by patchy pulmonary hypoxic vasoconstriction that leads to overperfusion in some areas. • This in turn to increased pulmonary capillary pressure (>18 mmHg) and capillary “stress” failure. • The exact mechanism for this hypoxic vasoconstriction is unknown. • Endothelial dysfunction due to hypoxia may play a role by impairing the release of nitric oxide. • Exercise and cold lead to increased pulmonary intravascular pressure and may cause HAPE
- 6. • Hypoxia triggered increase in sympathetic drive may lead to pulmonary venoconstriction and extravasation into the alveoli. • Inflammatory processes such as those elicited by a viral respiratory infection are shown to cause HAPE. • impaired transepithelial clearance of sodium and water from the alveoli.
- 7. References • Harrisons Principles of Internal Medicine, Volume 1. 21st edition. P3623-3626. • https://www.uptodate.com/contents/high-altitude-pulmonary- edema#H2
- 8. Acknowledgement • I gratefully acknowledge my teachers Dr. Mukesh Bairwa and Dr. Bimlesh for their valuable guidance, suggestions and support in preparing this presentation.