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Epoc y tabaco cmt
- 2. EPOC y Tabaco una guerra declarada CMGyF Centro Medico Toluca Marzo 2011 Dr Mario Hoyo
- 3. Muerte Guerra Hambre Victoria
- 11. Definición puntos a considerar • Prevenible • Tratable • Afectación sistémica • Inflamación sistémica
- 13. Reclutas
- 14. Reporte de Daños • La mortalidad se incremento del sexto lugar en 1990 a un estimado tercer lugar en el 2020 a nivel mundial. • En términos de morbilidad ocupara del cuarto al tercer lugar. • La prevalencia calculada en México para mayores de 40 años es de • Y en mayores de 60años asciende a
- 15. ¿Por Que cada vez mas Reclutas?
- 16. Daño en otros frentes
- 18. Reporte de Daños • Según el INEGI en el 2005 la epoc en mayores de 65 años se coloco en el quinto lugar dentro de las primeras 10 causas de muerte en México. • En morbilidad , en el INER la EPOC ocupa el segundo lugar como demanda en urgencias y es la cuarta causa de egreso hospitalario.
- 19. Arsenal • Según el censo general de población del 2000. el 56.9% de las viviendas rurales ocupan biomasa como energético. • Esto equivale a 14.5 millones de usuarios • Y cuatro de cada 10 viviendas cuentan con un solo cuarto. • El 37.5% de la población mayor de 40 años utiliza biomasa. • En el INER el 30% de los pacientes con epoc se debe a biomasa y mas del 88% son mujeres.
- 20. Estimación de Daños En cuestión de sobrevida según PLATINO • A los 3 años fallece el 20% • A los 6 años fallece el 30% • A los 8 años fallece el 40%
- 21. Costos de Guerra • Costos anuales en US es de 24 mil millones de dólares • En el 2000, 8 millones de consultas 1.5 millones de visitas a urgencias, 673 mil hospitalizaciones • Generando 18 mil millones de dólares por gastos directos. • Y 14 mil millones de dólares en gastos indirectos
- 23. Costos de Guerra • En costos de atención, la EPOC es 2.5 veces mas costosa contra otra enfermedad. • En México en el IMSS cifras por gastos anuales arrojan 73 303.00 por paciente, asciende a 139 978.00 si se hospitaliza • En el INER • 2 100.00 en CE día paciente • En hospitalización 2 290.00 • En urgencias 3 000.00 • En la UCI 40 000.00 • Al año 2 500 consultas, 350 hospitalizaciones gastan 13 millones de pesos, sin contar UCI.
- 24. ¿Por qué debemos dominar la EPOC? • Debido a que es un serio problema de salud publica. • Debido a su co-morbilidad con enfermedades de alta prevalencia. • Debido a su importante impacto económico • Debido a que es altamente incapacitante.
- 26. PATOGENESIS
- 29. Tabaco El cigarrillo contiene mas de 5000 compuestos diferentes 1015 radicales libres en su fase gaseosa Proceso inflamatorio crónico + agudizaciones
- 30. Trinchera
- 32. Sethi S and Murphy T. N Engl J Med 2008;359:2355-2365 Overview of Innate Defense in the Human Respiratory Tract
- 33. Barnes P. N Engl J Med 2000;343:269-280 Inflammatory Mechanisms in Chronic Obstructive Pulmonary Disease
- 34. Shapiro S. N Engl J Med 2005;352:2016-2019 Inflammatory-Cell Interactions in Chronic Obstructive Pulmonary Disease (COPD) and the Role of Histone Acetylation
- 35. Barnes P. N Engl J Med 2000;343:269-280 Oxidative Stress in Chronic Obstructive Pulmonary Disease
- 36. Cosio M et al. N Engl J Med 2009;360:2445-2454 Initial Response to Cigarette Smoke -- Step 1 in the Process Leading to COPD
- 37. Cosio M et al. N Engl J Med 2009;360:2445-2454 Proliferation of T Cells -- Step 2 in the Process Leading to COPD
- 38. Cosio M et al. N Engl J Med 2009;360:2445-2454 The Adaptive Immune Reaction -- Step 3 in the Process Leading to COPD
- 40. Cosio M et al. N Engl J Med 2009;360:2445-2454 Specimens from the Small Airways in the Healthy Lung of a Nonsmoker and the Lung of a Smoker with COPD
- 41. Diferentes Grados de Obstrucción en EPOC FEV1 > 80% FEV1/FVC > 70% ESPIROMETRIA NORMAL FLUJO L (seg) VOLUMEN (L) 1 2 3 4 5 1 2 3 4 5 VOLUMEN (L) VEF1 TIEMPO (seg) 1 2 3 4 5 1 2 3 4 5 FVC FEV1 > 80% FEV1/FVC < 70% OBSTRUCCION LEVE VOLUMEN (L) 1 2 3 4 5 FLUJO L (seg) 1 2 3 4 5 VOLUMEN (L) VEF1 TIEMPO (seg) FVC 1 2 3 4 5 1 2 3 4 5 FEV1 = 30- 50% FEV1/FVC < 70% OBSTRUCCION MODERADA VOLUMEN (L) FLUJO L (seg) 1 2 3 4 5 1 2 3 4 5 VOLUMEN (L) VEF1 TIEMPO (seg) FVC 1 2 3 4 5 1 2 3 4 5 VOLUMEN (L) FEV1 < 30% FEV1/FVC < 70% OBSTRUCCION SEVERA TIEMPO (seg) FLUJO L (seg) VOLUMEN (L) 1 2 3 4 5 1 2 3 4 5 VEF1 FVC 1 2 3 4 5 1 2 3 4 5
- 42. H. Wenske International Training BI VT ERV IC RV Mild COPD at rest Mild COPD at rest, during exercise, and after exercise Mild COPD after exercise Dynamic Hyperinflation Mild COPD during exercise Start exercise
- 44. • BTP 50-80% ;30-49%; -30% • ATS-ERS mismas de GOLD sin muy severo
- 45. II: Moderada Agregar tratamiento de mantenimiento con broncodilatador de acción larga (anticolinérgicos, B2AAP) más rehabilitación III: Grave Intentar con corticosteroides inhalados si hay exacerbaciones frecuentes y xantinas I: Leve Disminuir factores de riesgo: Vacunación influenza Usar b2 de acción corta por razón necesaria IV: Muy grave Agregar oxígeno continuo si hay falla respiratoria. Considerar tratamiento quirúrgico.Y VMNI. Terapia en cada estadio de la EPOC GOLD 2007
Notas del editor
- Huprey Bougard (casa Blanca) El cigarrillo,la guerra y la post guerra
- Luther Terry Cirujano General (secretario de salud de USA) en 1963 anuncia con mas de 2000 trabajos bajo evidencia que el tabaco es un producto nocivo para la salud.
- Delgada linea roja
- Darwin no solo nos relaciono fisicamente con los simios sino tambien conductualmente.
- Pintada en 1886 pocos antes de su muerte en 1890
- Estudios mexicanos e indues integraron a gold como factor de riesgo al humo de leña
- El negocio mas lucrativo en los años venideros serán los asilos de ancianos
- Platino estudio epidemiológico latinoamericano, análogo al estudio NICE y BOLD (ATS y ERS)
- El 6 de junio de 1944 se desarrolla la movilización militar anfibia mas grande de todos los tiempos participan 50mil soldados En el primer desembarque morirán 2500 hombres ese día en total (2 de cada 10) y se embarcaran 2 millones. Se instalan 5 cabezas de playa utha y omaha con USA, gold sword RU , juno canadienses.
- A partir de un estimulo-----hay lesión tisular y como consecuencia remodelación
- Estimulo agresor Ligting livereitor
- Agresión tisular
- Son tres niveles en los que participa la agresion tisular, 1)epitelio de vias aereas centrales,2) lesion en vias aeres perifericas 3)cambios inflamatorios a nivel alveolar, gestado por una inmunidad innata ineficiente donde participan diferentes mediadores(mucina peptidos iga) Figure 2. Overview of Innate Defense in the Human Respiratory Tract. Predominant defense mechanisms for large airways, for both large and small airways, and for alveoli are depicted; some mechanisms are operative at multiple sites. Cells that participate in innate immunity include ciliated epithelial cells, goblet cells, dendritic cells, airway macrophages, alveolar macrophages, neutrophils, and pneumocytes. Secreted products that contribute to innate immunity include antimicrobial peptides, inflammatory mediators, mucin, and secretory IgA.
- Figure 3. Inflammatory Mechanisms in Chronic Obstructive Pulmonary Disease. Cigarette smoke and other irritants activate macrophages and airway epithelial cells in the respiratory tract, which release neutrophil chemotactic factors, including interleukin-8 and leukotriene B4. Neutrophils and macrophages then release proteases that break down connective tissue in the lung parenchyma, resulting in emphysema, and also stimulate mucus hypersecretion. Proteases are normally counteracted by protease inhibitors, including {alpha}1-antitrypsin, secretory leukoprotease inhibitor, and tissue inhibitors of matrix metalloproteinases. Cytotoxic T cells (CD8+ lymphocytes) may also be involved in the inflammatory cascade. MCP-1 denotes monocyte chemotactic protein 1, which is released by and affects macrophages.
- Figure 1. la destruccion de la matriz alveolar es propuesta por la acetilacion de histonas que desempacan el dna y promueven la inflamacion. A travez del bloqueo inhibidor kb y liberacion del factor nuclear kb. Por otro lado los cd8 y los PMN acentuan el desequilibrio de proteasas. antiproteasa. Inflammatory-Cell Interactions in Chronic Obstructive Pulmonary Disease (COPD) and the Role of Histone Acetylation. Reactive oxygen species resulting from inhaled cigarette smoke (and potentially from the inflammatory cells themselves) promote transcription of nuclear factor-{kappa}B (NF-{kappa}B)-mediated proinflammatory factors by way of two mechanisms. First, oxidation results in the degradation of IK-{kappa}B, releasing NF-{kappa}B, which then translocates to the nucleus of the targeted cell. Oxidation also inactivates histone deacetylase (HDAC), shifting the balance to increased DNA acetylation, weakening the interactions between histone and DNA and "unwinding" DNA, allowing NF-{kappa}B greater access to the DNA promoter elements, and leading to transcription of neutrophil chemokines and cytokines (tumor necrosis factor {alpha} [TNF-{alpha}] and interleukin-8) and matrix metalloproteinases (MMPs). These factors recruit and activate neutrophils to the lung. In addition, CD8+ T cells augment the production of macrophage MMPs through interactions with surface-bound CD40 molecules and interferon-inducible chemokines (inducible protein of 10 kD [IP-10], interferon-inducible T-cell alpha chemoattractant [I-TAC], and monokine induced by interferon-{gamma} [MIG]). Macrophage MMPs and neutrophil elastase degrade each other's inhibitors, the tissue inhibitor of metalloproteinases and alpha1-antitrypsin, respectively, augmenting their matrix-degrading capacities. These interactions illustrate the highly interactive nature of the immune inflammatory response and suggest that breaking this cycle, perhaps by way of augmentation of HDAC with the use of theophylline, may prevent inflammatory-mediated destruction of the lung in COPD. Dashed lines indicate inhibition.
- Figure 5. Estres oxidativo de radicales libres de oxigeno superoxidos, peroxidos de hidrgeno, hidroxílos y peroxinitratos. Oxidative Stress in Chronic Obstructive Pulmonary Disease. Reactive oxygen species from cigarette smoke or from inflammatory cells have several damaging effects, including decreased antiprotease defenses; activation of nuclear factor-{kappa}B, resulting in increased secretion of the cytokines interleukin-8 and tumor necrosis factor {alpha}; increased production of isoprostanes; and direct effects on airway functions. O2- denotes superoxide anion, H2O2 hydrogen peroxide, OH{middle dot} hydroxyl radical, and ONOO- peroxynitrate.
- Figure 3.¿ Por que se perpetua la el estimulo lesional en estadios I de GOLD? el responsable es el TLR (recetores similares a campana). Al actuar en el epitelio de la respuesta innata. Initial Response to Cigarette Smoke -- Step 1 in the Process Leading to COPD. Cigarette smoke injures epithelial cells, which release "danger signals" that act as ligands for toll-like receptors (TLRs) in the epithelium. These actions trigger the production of chemokines and cytokines, which results in an innate inflammation. Products from the inflammatory cells may injure the extracellular matrix, leading to the release of TLR ligands and consequent TLR activation, which will promote further inflammation, tissue injury, and the production of antigenic substances. This chain of events may cause dendritic cells to mature and migrate to local lymph organs, where, if the conditions are favorable, T-cell activation may result, with progression of the disease. If the innate inflammation in step 1 is minimized or controlled, the inflammation will not progress to adaptive immunity, and the disease may be arrested. These processes are typical of smokers who have neither COPD nor Gold stage 1. GM-CSF denotes granulocyte-macrophage colony-stimulating factor, HSP heat-shock protein, ICAM-1 intercellular adhesion molecule 1, MCP-1 monocyte chemoattractant protein 1, and TNF tumor necrosis factor.
- Figure 4. en el estadio II de gold las celulas desdriticas migran al pulmon gestando reclutamiento de celulas inflamatorias. Proliferation of T Cells -- Step 2 in the Process Leading to COPD. When step 1 is successful, mature dendritic cells migrate to local lymphatic organs, whereupon stimulation by toll-like receptors (TLRs) leads to the expression of CD80-CD86 and cytokines, creating a propitious milieu for T-cell antigen presentation and proliferation into effector CD4+ type 1 helper (Th1) T cells and cytolytic CD8+ T cells. Interleukin-6, secreted by the dendritic cells, favors the production of effector T cells by overcoming the signals from regulatory T (Treg) cells. Upon activation, effector T cells express tissue-specific chemokine receptors. Immune regulation or tolerance mechanisms will determine at this stage the degree of proliferation of T-cell effectors, homing, and eventually, disease severity. An absence of tolerance is associated with Gold stage 3 or stage 4, moderate tolerance with Gold stage 2, and full tolerance with Gold stage 1. MHC denotes major histocompatibility complex.
- Figure 5. En el estadio 3 de GOLD practicmante los linfocitos T promueven una inmunidad adaptativa que perpetua el mensaje inicial y con ello el daño. The Adaptive Immune Reaction -- Step 3 in the Process Leading to COPD. With the failure of tolerance or immune regulation in step 2, an adaptive immune inflammation (autoimmune) develops in the lung, consisting of CD4+ type 1 helper (Th1) T cells, cytolytic CD8+ T cells, and IgG-producing B cells. Regulatory T cells (Treg) and {gamma}{delta} CD8+ T cells could modulate the severity of the adaptive immune inflammation. The resulting immune inflammation, induced by CD4+ Th1 T cells and consisting of activated innate immune cells producing oxidative stress and proteinases, along with cytolytic CD8+ T cells and B cells, leads to cellular necrosis and apoptosis, immune and complement deposition, tissue injury with airway remodeling, and emphysema, as well as the release of additional antigenic material, which perpetuates the process. In step 3, the full autoimmune process has developed, producing the most severe disease (Gold stage 3 and stage 4). NO denotes nitric oxide, and ROS reactive oxygen species.
- Culmina en una plena remodelacion del campo de batalla
- Figure 1. Specimens from the Small Airways in the Healthy Lung of a Nonsmoker and the Lung of a Smoker with COPD. In the specimen of the small airways (membranous bronchioles) from the healthy lung of a nonsmoker (Panel A), the airway walls are thin, and intact alveoli are attached along its circumference. In a comparable specimen from the lung of a smoker with COPD (Panel B), the diameter of the airway is narrowed, the airway wall is thickened, and many of the alveolar attachments are broken. CD8+ T lymphocytes (in red) infiltrate the airway wall in the specimen from the smoker with COPD (Panel B) but not in the specimen from the nonsmoker (Panel A) (immunostaining with antihuman CD8; counterstained with hematoxylin). Images courtesy of Dr. Fiorella Calabrese.
- Esta tabla presenta de manera resumida el tratamiento en cada estadio de la EPOC. Es resultado del consenso mundial de expertos sobre la enfermedad