Disease Pathophysiology Discussion

Myocardial Infarction

Refers to irreversible necrosis of the myocardium following prolonged ischemia. Ischemia results in myocyte changes such as myofibril relaxation, sarcolemmal disruption, and mitochondrial alteration which leads to coagulative necrosis of the myocardium (McCance & Huether, 2019). Similarly, the intense inflammatory response results in apoptosis and myocardial fibrosis due to the limited regenerative capacity of the myocytes. Ultimately, impairment of cardiac function ensues influenced by the region affected. The remaining viable myocardium undergoes segmental hypertrophy and dilatation.

Endocarditis

Endocarditis refers to infectious/noninfectious inflammation of the endocardial lining of a heart valve, a cardiac chamber, or a great blood vessel with the formation of vegetation (Rajani & Klein, 2020). Infective endocarditis originates from bacterial invasion and colonization of sterile fibrin-platelet vegetation. Known risk factors for endocarditis include damaged heart valves, congenital heart defects, IV drug users, prolonged cardiac catheterization, poor dental health, artificial cardiac devices, and old age (Rajani & Klein, 2020). Left untreated, endocarditis may cause heart failure, heart valve destruction, stroke, and even pulmonary embolism among other complications.

Myocarditis

Myocarditis refers to the inflammation of the myocardium. It is predominantly seen in younger patients (McCance & Huether, 2019). Myocarditis can be infectious or noninfectious. Infectious myocarditis with viral etiology is the most common cause. Invasion of the myocyte by viral pathogen activates both innate and adaptive immunity. However, this may be exaggerated leading to chronic inflammation, myocardial remodeling, and ventricular dysfunction.

Valvular Disorders

Valvular disorders are broadly congenital or acquired. They occur when one or more heart valve is unable to open or close effectively. Valvular disorders take the form of stenosis when the valve cannot open sufficiently, regurgitation when the valve becomes leaky due to incomplete closure, and prolapse when the valve leaflets slip out of their place. These aforementioned functional abnormalities occur largely as a consequence of aging.

Lipid Panel

The lipid profile outlines HDL cholesterol, LDL cholesterol, triglyceride, and total cholesterol (Sun et al., 2020). Common indications for a lipid panel include pancreatitis, screening for lipid disorders in the presence of family history, evaluation for lipid-lowering therapy, the establishment of the 10-year cardiovascular risk, and management of atherosclerotic cardiovascular diseases (Sun et al., 2020). Finally, a fasting blood specimen produces optimal results.

Coagulation

Coagulation is considerably a dynamic process that entails a cascade of events leading to hemostasis at the site of vascular injuries (Sang et al., 2021). It involves a complex interplay between platelets, blood vessel wall, and coagulation cascade. The initial step is arteriolar vasoconstriction mediated by endothelin and neurogenic reflex. Subsequently, primary hemostasis occurs characterized by platelet adhesion, activation, and aggregation followed by secondary hemostasis due to the coagulation cascade (Sang et al., 2021). The final step involves clot stabilization and remodeling.

Clotting Cascade

The clotting cascade consists of intrinsic and extrinsic pathways which congregate at factor X activation leading to the common pathway. The cascade entails enzymatic activation events in which serine proteases activate proenzymes and procofactors in the subsequent step of the cascade via limited proteolysis. The ultimate result is the polymerization of fibrin and activation of platelets leading to blood clot formation.

Deep Vein Thrombosis

DVT is a demonstration of venous thromboembolism. DVT is an interplay between venous stasis, endothelial damage, and a hypercoagulable state (McCance & Huether, 2019). Venous stasis results in an increase in viscosity and microthrombi. Endothelial damage, on the other hand, stimulates an inflammatory response and activation of the coagulation system while a hypercoagulable state stems from biochemical disequilibrium between circulating factors. Early thrombus interaction with the endothelium promotes leucocyte adhesion and cytokine production resulting in DVT. The ultimate propagation of the clot is contingent on the parallelism between thrombolytic and coagulation pathways.

Hypertension

Hypertension is characterized by persistently elevated systolic blood pressure of 140 mmHg or more and/or diastolic blood pressure of 90 mmHg or more (Brouwers et al., 2021). Irrespective of the etiology, ultimate changes that lead to hypertension include an increase in total peripheral resistance and afterload. According to Brouwers et al. (2021), the pathophysiology of hypertension is intricate and involves underlying mechanisms such as volume expansion, impaired RAAS response, and enhanced activation of the sympathetic nervous system.

Heart Failure

In heart failure, the heart, through abnormality of cardiac function, is incapable of pumping blood to meet the metabolic requirements of the body (Schwinger, 2021). Regardless of the etiology, heart failure ensues only when compensatory mechanisms become overwhelmed. These adaptations include the Frank-Starling mechanism, changes in myocyte regeneration and death, activation of the neurohormonal system, myocardial hypertrophy, and cardiac chamber dilatation. Diminished ventricular compliance and diastolic ventricular dysfunction result in heart failure with preserved ejection fraction while systolic dysfunction and diminished contractility results in heart failure with reduced ejection fraction (Schwinger, 2021).

COPD

COPD is a progressive disease state characterized by incompletely reversible airflow limitation and an abnormal inflammatory response to inhaled noxious particles. Most cases of COPD result from exposure to cigarette smoke. In chronic bronchitis, irritants induce an inflammatory response and hypertrophy of mucus glands leading to bronchiolar wall fibrosis and mucus hypersecretion, respectively. Meanwhile, in emphysema, irritants stimulate protease-antiprotease and oxidant-antioxidant imbalances leading to loss of elastic recoil and depletion of local antioxidants, respectively.

Asthma

The pathophysiology of asthma is complex and encompasses an interplay between intermittent airway obstruction, bronchial hyperresponsiveness, and airway inflammation (Bush, 2019). Bronchial hypersensitivity is responsible for the inflammatory response and mucus production after inhalation of an allergen. However, airway obstruction stems mainly from mucus plug, bronchoconstriction, and inflammatory cell infiltration. If not well controlled, irreversible changes in the airway may result, distinguished by epithelial desquamation, alveolar basement thickening, and bronchial smooth muscle hyperplasia.

Pneumonia

Pneumonia is an infection of the lung (Lim, 2020). It can be bacterial, viral, or fungal. Pneumonia occurs when the virulence factors of an invading pathogen overwhelm both local and systemic host defense mechanisms of both innate and adaptive immunity. The result is an inflammatory process that leads to exudative congestion, diminished lung compliance, ventilation-perfusion mismatch, and increased diffusion distance (Lim, 2020). Consequently, the gaseous exchange is impaired, leading to hypoxemia.

 

 

References

Brouwers, S., Sudano, I., Kokubo, Y., & Sulaica, E. M. (2021). Arterial hypertension. Lancet398(10296), 249–261. https://doi.org/10.1016/S0140-6736(21)00221-X

Bush, A. (2019). Pathophysiological mechanisms of asthma. Frontiers in Pediatrics7, 68. https://doi.org/10.3389/fped.2019.00068

Lim, W. S. (2020). Pneumonia—Overview. In Reference Module in Biomedical Sciences. Elsevier. https://doi.org/10.1016/b978-0-12-801238-3.11636-8

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.

Rajani, R., & Klein, J. L. (2020). Infective endocarditis: A contemporary update. Clinical Medicine (London, England)20(1), 31–35. https://doi.org/10.7861/clinmed.cme.20.1.1

Sang, Y., Roest, M., de Laat, B., de Groot, P. G., & Huskens, D. (2021). Interplay between platelets and coagulation. Blood Reviews46(100733), 100733. https://doi.org/10.1016/j.blre.2020.100733

Schwinger, R. H. G. (2021). Pathophysiology of heart failure. Cardiovascular Diagnosis and Therapy11(1), 263–276. https://doi.org/10.21037/cdt-20-302

Sun, J. T., Chen, Z., Nie, P., Ge, H., Shen, L., Yang, F., Qu, X. L., Ying, X. Y., Zhou, Y., Wang, W., Zhang, M., & Pu, J. (2020). Lipid profile features and their associations with disease severity and mortality in patients with COVID-19. Frontiers in Cardiovascular Medicine7, 584987. https://doi.org/10.3389/fcvm.2020.584987

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