Pathophysiology of COPD - Buzzle

Peroxidative degradation of lipids yields the highly reactive aldehyde 4-hydroxy-2-nonenal (4-HNE), a major product of the lipid peroxidation. 4-HNE triggers cell signaling by reacting and forming adducts with sensor proteins and thus initiating or inhibiting cell response pathways (). Rahman et al. () reported enhanced immunohistochemical detection of 4-HNE-modified proteins in airway and alveolar epithelial cells, endothelial cells, and neutrophils in subjects with COPD, when compared with subjects without COPD. Interestingly, these investigators also found a significantly inverse correlation between FEV1 and the levels of 4-HNE adducts in alveolar epithelium, airway endothelium, and neutrophils. Increased levels of 4-HNE adducts were also observed in bronchiolar epithelial and alveolar epithelial cells, particularly type II cells in male C57BL/6 mice after 1 h of cigarette smoke exposure (). Exposure of bovine lung microvascular endothelial cells to 4-HNE decreased endothelial cell permeability via phosphorylation of JNK, ERK, and p38 MAPK, with no evidence of apoptosis (). However, 4-HNE was reported to induce JNK-mediated apoptosis in a variety of other cell lines (). Physiologically relevant concentrations of 4-HNE inhibited transcriptional activation of NF-κB by preventing IκBα phosphorylation in cultured Kupffer cells treated with Chlamydia pneumoniae () and in human monocytic lineage cells treated with LPS (). Because the increase of 4-HNE may represent a useful oxidative stress marker, and is responsible for signal transduction and apoptosis, further studies are needed to clarify its role in the pathophysiology of COPD.

Pathophysiology of COPD | allnurses

Pathophysiology of COPD - YouTube

Pathophysiology of COPD - EzineArticles

EFL is a pathophysiological hallmark of COPD. Patients with COPD are said to be flow limited when the expiratory flow they generate during tidal respiration represents the maximal possible flows that they can generate at that volume. In flow limited patients the time available for lung emptying (expiratory time) during spontaneous breathing is often insufficient to allow end expiratory lung volume (EELV) to decline to its natural relaxation volume leading to lung overinflation. Thus, in flow limited patients, EELV becomes dynamically rather than statically determined, and essentially becomes a continuous variable that fluctuates widely depending on the extent of EFL and the prevailing ventilatory demand. Dynamic hyperinflation (DH) refers to acute and variable increase in EELV above its baseline value. DH occurs during exercise in flow limited patients as inspired tidal volume increases and expiratory time decreases, and is associated with severe mechanical constraints on ventilation and perceived respiratory discomfort. DH also occurs during acute bronchoconstriction in asthma. In this setting, the reduction in inspiratory capacity (IC), which reflects the increase in EELV, correlates strongly with the perception of inspiratory difficulty.,

The pathophysiology of COPD is not completely understood.

The pathophysiology of severe COPD exacerbations requiring mechanical ventilation is now well understood. Increased airways resistance, usually as a result of worsening airway inflammation, results in critical EFL and DH with dramatically increased loading and functional weakness of the inspiratory muscles. The accessory muscles of breathing are maximally recruited and significant thoracoabdominal dysynchrony is often evident. Inspiratory threshold loads increase substantially (values between 13 and 20 cm H2O have been recorded) and this has been suggested to account for nearly 60% of the increased static inspiratory work of breathing during an exacerbation.,,, Dynamic lung compliance becomes precipitously reduced as a result of the accompanying tachypnoea (and reduced inspiratory time) and, in conjunction with the increased airways resistance, also contributes importantly to the increased dynamic inspiratory work.,,,,

Pathophysiology of COPD
Pathophysiology Of Copd Pictures

Pathophysiology Of Copd Powerpoint

In view of the persuasive evidence presented above that oxidative stress is important in the pathophysiology of COPD, antioxidants are a logical approach to therapy (; ).

Pathophysiology of the COPD Exacerbation - Hilary Cain MD

What Is the Pathophysiology of COPD? - Healthline

Structural changes in COPD initiate instability in pulmonary hemodynamics. Most moderate-to-severe COPD patients develop some degree of mild PAH (25-35 mmHg) over the course of time, and rarely severe PAH (>45mmHg),20 however, it may be a rare accompaniment of mild-moderate COPD cases. PAH is a known independent prognostic marker of COPD. Each episode of COPD exacerbation increases pulmonary arterial pressure by 20mmHg which can develop into full fledged PAH on recurrent episodes. PAH primarily depends on pulmonary artery wedge pressure plus product of cardiac-output and pulmonary-resistance. Pathophysiological consequences of COPD such as hypoxia, hyperinflation, emphysema, hypoxia-induced secondary polycythemias and lung and systemic inflammation can induce pulmonary capillary muscularization, intimal-wall thickenings, plexiform lesions, endothelial dysfunctions and apoptosis which can potentially generate enhanced pulmonary vascular resistance which predisposes PAH.20 Increased intrathoracic pressures in emphysema induce positive pressures on right ventricle resulting in increased pulmonary artery wedge pressure. Left ventricular diastolic dysfunction secondary to cardiovascular morbidities in COPD can also cause back pressure changes in pulmonary vasculature and right ventricles. Chronic severe pulmonary hypertension increases right ventricular after-load and eventually leads to the clinical syndrome of right heart failure with systemic congestion and inability to adapt right ventricular output to peripheral vascular demands (Figure 5).

Pathophysiology of COPD - Coalition for Pulmonary Fibrosis

The Airway Pathophysiology of COPD - Taylor & Francis Online

Inflammation in COPD is complex, with many activated inflammatory and structural cells that release multiple mediators, including lipid mediators such as LTB4, which is chemoattractant for neutrophils; chemokines such as MCP-1 and MIP-1α, which attract monocytes; IL-8 and GRO-α, which attract neutrophils and monocytes; IP-10, which attracts CD8+ cells, ROS, and NO; GM-CSF, which prolongs neutrophils' survival; TNF-α, which amplifies inflammation by switching on multiple inflammatory genes and may also account for some of the systemic effects of the disease; and endothelin and TGF-β, which induce fibrosis. In addition, multiple proteinases are released that result in elastolysis, including the serine proteinases neutrophils elastase and proteinase C, cathepsins, and MMPs. This combination of mediators that attract and activate inflammatory cells and proteinases, which cause elastolysis and mucus hypersecretion, results in the typical pathophysiology of COPD.