Respirology BMS 250 True or False

The ACE2 enzyme binds to the spike protein of SARS-CoV-2 to allow viral entry into cells.

Thrombotic sequelae are common in COVID-19 patients due to excessive bleeding tendencies.

The Renin-Angiotensin-Aldosterone System (RAAS) is not involved in the pathophysiology of COVID-19.

Proinflammatory cytokines like TNF-α and IL-6 are secreted in a cytokine storm during COVID-19, causing harm to multiple organ systems.

Vascular leakage in the lungs is not associated with acute respiratory distress syndrome (ARDS) in COVID-19 patients.

The activation of kinin receptors on the lung endothelium leads to vascular smooth muscle contraction.

Viral uptake can be promoted by the cleavage of ACE2 by TMPRSS2.

Dysregulated proinflammatory cytokine release does not contribute to the processes leading to pulmonary edema in COVID-19.

Microthrombi formation frequently occurs due to anomalous coagulation and can lead to thrombotic sequelae in COVID-19.

The renin-angiotensin-aldosterone system has no involvement in the pathophysiology of COVID-19.

Influenza A and influenza B are positive-sense single-stranded RNA viruses.

In most cases, the host's immune response is not able to control and eliminate the virus, leading to recovery from influenza illness within a week or two.

The Neuraminidase spike in influenza helps the virus bind to and invade the host cell.

Excessive inflammation and cytokine release during influenza infection never contribute to the severity of symptoms and complications.

Thrombotic sequelae are often observed in patients with pleural effusions.

Individuals with weakened immune systems are less likely to progress to severe complications like bacterial pneumonia during influenza infection.

The pathogenesis of influenza involves a static interaction between the virus and the host's immune response.

Vascular leakage in the lungs is a common feature of the pathogenesis of influenza.

Inflammation and tissue damage never occur in the respiratory tract during influenza infection.

The Renin-angiotensin-aldosterone system plays a significant role in the immunity against influenza viruses.

Parapneumonic effusion typically arises when the infection spreads to the lungs, causing inflammation and fluid buildup.

Empyema is a collection of blood within the pleural cavity that can develop if a parapneumonic effusion is left untreated.

The exudative phase of parapneumonic effusion is characterized by sterile fluid rich in protein due to increased pleural and vascular permeability.

The organization stage of parapneumonic effusion is characterized by elastic membrane formation that facilitates easy lung inflation.

Parapneumonic effusion is commonly seen in viral pneumonia cases.

Influenza viruses primarily infect the gastrointestinal tract.

The virus enters the host's respiratory tract only through inhalation of respiratory droplets.

After entering the host cell, the viral RNA is released into the nucleus for replication.

Influenza infection can lead to thrombotic sequelae in some cases.

The host's immune system in response to influenza infection does not involve activation of innate immune cells.

Vascular leakage in the lungs is not associated with acute respiratory distress syndrome (ARDS) in patients with severe influenza infections.

Thrombotic sequelae are common in patients with severe influenza infections due to excessive bleeding tendencies.

The Renin-Angiotensin-Aldosterone System (RAAS) is not involved in the pathophysiology of influenza infections.

Activation of cytotoxic T cells is the primary mechanism for eradicating the influenza virus from the body.

Proinflammatory cytokines like TNF-α and IL-6 are secreted in a cytokine storm during severe influenza infections.

Antibodies play a minor role in clearing the influenza virus but are crucial for providing long-term immunity against future infections.

Thrombotic sequelae are rare in patients with severe influenza infections.

The primary immune response to influenza is mediated by B cells.

Influenza A viruses can undergo both antigenic drift and antigenic shift, leading to the emergence of new strains.

Influenza B viruses have a higher epidemic potential compared to Influenza A viruses.