"Unveiling the Lethal Mechanisms: How COVID-19 Claims Lives"

"Unveiling the Lethal
Mechanisms: How COVID-19 Claims Lives"

Introduction

COVID-19, commonly known as the "coronavirus," technically named SARS-CoV-2, has become a familiar and profoundly impactful presence worldwide. Its spread has caused widespread tragedy and significant mental distress as a global pandemic. 


Here we can explore the intricate mechanisms through which COVID-19 exerts its lethal effects on the human body. By understanding viral pathology, host immune response, and systemic complications, we can gain a deeper insight into the factors that contribute to the mortality of this unprecedented viral threat. 

Spread

Since it's an airborne virus, COVID-19 spreads through droplets of contaminated body fluids, much like many other airborne viruses like influenza etc.... 


Its mode of transmission is direct contact with infected people which may be through  sneezing, coughing and talking of infected individuals. A single sneeze can produce at least 40,000 droplets, highlighting the potential for widespread transmission of the virus. Or indirect through surface or objects of immediate environment. 

Entry

Touching of contaminated hand to a person's mouth, nose or eyes Upon inhalation the virus attaches to the mucous membranes lining the nose, mouth, and throat. 

Infection

Initially Sars cov2 Infects the pharyngeal epithelium and induces inflammation which accounts for flu like symptoms at the beginning. 

In the lungs the virus progress infection by binding to angiotensin converting enzyme 2 (ACE2) receptors on the surface of type 2 alveolar cells which are responsible for producing surfactants. These surfactants lowers the surface tension thus preventing alveolar collapse. 

Symptoms

Mild : Influenza like symptoms which include fever, chills, muscle aches, cough, congestion, runny nose, headaches, fatigue etc....


Severe : Acute respiratory distress syndrome


ACE2 receptors are present on type II alveolar cells, which normally produce surfactants to reduce alveolar surface tension. Damage to these cells can lead to reduced surfactant production and increased surface tension. 

This disruption affects the balance between the air inside the alveoli and the liquid lining the alveolar walls, leading to fluid retention in the interstitial space. Consequently, this disturbance impairs gas exchange and causes respiratory distress.

Immunological reactions

There occurs a phenomenon known as cytokine strome exhibited by by our immune cells like the neutrophils and lymphocytes and the macrophages
will lead to increased production of interleukins, interferon like IL - 2,6,7,8,10 , TNF - alpha , INF - gamma.
This will lead to The elevated cytokines leads to various consequences such as:
Tissue damage and necrosis
Impaired gas exchange, leads to tissue hypoxia
Endothelial damage of pulmonary vasculature, leading to vasodilation, microvascular thrombosis and hemorrhage, and hypercoagulability
Dilatation of blood vessels underlying the alveoli: This allows passage of fluid from the blood vessels to lungs which leads to pulmonary edema. 

Multi organ failure

Cytokines can also induce damage to other organs of the body such as heart, kidney, liver, etc. There occur events such as sepsis, septic shock and multiorgan failure including acute kidney injury and cardiac injury during to cytokines.

Risk population 

Age > 60 years (risk increases with age)
Patients with Underlying comorbidities such as diabetes, hypertension, cardiac disease, chronic obstructive lung disease (COPD), cerebrovascular disease, chronic kidney disease, immune-suppression (eg : AIDS) and cancer

Death



Death in COVID-19 is primarily due to 
●Acute respiratory distress syndrome (ARDS), ●Sepsis
●Multi-organ failure
●Thromboembolic events. 
●Lung damage - respiratory failure. 








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