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COVID-19 for ABIM

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COVID-19 for American Board of Internal Medicine
Etiology
  • SARS-CoV-2:
    • COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus first identified in 2019. It belongs to the Coronaviridae family, which also includes the viruses responsible for SARS and MERS.
    • SARS-CoV-2 is an enveloped, single-stranded RNA virus with spike proteins that bind to the angiotensin-converting enzyme 2 (ACE2) receptor, facilitating viral entry into host cells.
  • Variants:
    • Multiple variants of SARS-CoV-2 have emerged due to mutations in the spike protein, leading to changes in transmissibility, immune escape, and virulence. Examples include the Alpha, Delta, and Omicron variants.
Transmission
  • Respiratory Droplets:
    • COVID-19 is primarily transmitted via respiratory droplets from coughs, sneezes, or talking. Close contact with an infected individual or inhalation of aerosols can also spread the virus.
  • Aerosol Transmission:
    • In poorly ventilated spaces, smaller particles (aerosols) can remain suspended in the air, increasing the risk of airborne transmission, particularly in close indoor settings.
  • Fomite Transmission:
    • Although less common, SARS-CoV-2 can be transmitted via contact with contaminated surfaces followed by self-inoculation of the mucous membranes (eyes, nose, mouth).
Pathophysiology
  • Viral Entry:
    • SARS-CoV-2 enters host cells by binding to the ACE2 receptor, which is expressed in multiple tissues, including the respiratory epithelium, lungs, and endothelial cells. This widespread ACE2 distribution accounts for the multisystem involvement of COVID-19.
  • Immune Response:
    • Infection triggers both innate and adaptive immune responses. Severe disease can result from dysregulated immune responses, including a cytokine storm, where excessive release of pro-inflammatory cytokines (e.g., IL-6, TNF-α) causes widespread tissue damage and contributes to acute respiratory distress syndrome (ARDS), multi-organ failure, and coagulopathy.
  • Coagulopathy:
    • COVID-19 is associated with a prothrombotic state characterized by elevated D-dimer and thrombosis (e.g., deep vein thrombosis, pulmonary embolism). Microvascular thrombosis contributes to complications like ARDS and organ dysfunction.
Clinical Features
  • Incubation Period:
    • The incubation period is typically 2-14 days after exposure, with a median of 4-5 days.
  • Mild to Moderate Disease:
    • Symptoms include:
    • Fever and chills (most common initial symptoms)
    • Cough (usually dry but may become productive)
    • Fatigue
    • Myalgias
    • Sore throat
    • Headache
    • Anosmia and ageusia (loss of smell and taste, common in early stages)
    • Gastrointestinal symptoms (nausea, diarrhea, abdominal pain) are less common.
  • Severe Disease:
    • Approximately 15-20% of symptomatic patients progress to severe disease, characterized by:
    • Dyspnea and hypoxia (SpO2 < 94%)
    • Pneumonia: May lead to acute respiratory distress syndrome (ARDS).
    • Cytokine storm: Excessive inflammation can result in multi-organ failure.
  • Critical Disease:
    • A small percentage of patients develop critical disease, including:
    • ARDS
    • Septic shock
    • Multi-organ dysfunction
Diagnosis
  • PCR Testing:
    • Reverse transcription-polymerase chain reaction (RT-PCR) from nasopharyngeal or oropharyngeal swabs is the gold standard for diagnosing SARS-CoV-2 infection. It detects viral RNA and is highly sensitive and specific.
  • Antigen Testing:
    • Rapid antigen tests detect viral proteins and provide quicker results but are less sensitive than PCR, especially in asymptomatic individuals or early in infection.
  • Chest Imaging:
    • Chest X-ray: May show bilateral, peripheral opacities, typically associated with pneumonia.
    • Chest CT: More sensitive and may reveal ground-glass opacities and consolidation in early or severe disease.
  • Laboratory Findings:
    • Common laboratory abnormalities in severe disease include:
    • Lymphopenia
    • Elevated D-dimer (associated with worse prognosis)
    • Elevated C-reactive protein (CRP) and ferritin
    • Elevated liver enzymes (AST/ALT)
    • Elevated troponins in cases with myocardial involvement.
Management
Mild to Moderate Disease
  • Supportive Care:
    • Management includes antipyretics (e.g., acetaminophen), hydration, and isolation to prevent transmission. Most patients can be managed at home.
  • Antiviral Therapy:
    • Nirmatrelvir-ritonavir (Paxlovid) and remdesivir are antivirals that may reduce the severity of illness if administered early in high-risk individuals.
  • Monoclonal Antibodies:
    • Monoclonal antibodies (e.g., sotrovimab) are used for early treatment in high-risk patients to prevent progression to severe disease.
Severe to Critical Disease
  • Hospitalization:
    • Patients with hypoxia (SpO2 < 94%) or worsening symptoms should be admitted for closer monitoring and supportive care, including oxygen supplementation.
  • Corticosteroids:
    • Dexamethasone (6 mg daily for up to 10 days) is recommended for patients with severe or critical illness requiring supplemental oxygen or mechanical ventilation. It reduces mortality by modulating the inflammatory response.
  • Antivirals:
    • Remdesivir is an antiviral given to hospitalized patients with severe COVID-19, reducing the duration of illness, particularly in those requiring supplemental oxygen.
  • Immunomodulators:
    • Tocilizumab, an IL-6 receptor antagonist, may be used in patients with cytokine storm or severe inflammatory responses.
  • Anticoagulation:
    • Prophylactic anticoagulation is recommended in all hospitalized patients due to the high risk of thromboembolic events. Therapeutic anticoagulation may be considered for documented thrombotic events.
Complications
  • Respiratory Failure:
    • Progression to ARDS is the most feared complication, requiring mechanical ventilation and intensive care.
  • Cardiovascular Complications:
    • Myocarditis, heart failure, arrhythmias, and thromboembolic events (e.g., pulmonary embolism).
  • Neurologic Complications:
    • Stroke, encephalopathy, and long-term neurological sequelae (e.g., cognitive impairment) are seen in severe disease.
  • Post-COVID Syndrome:
    • Persistent symptoms (e.g., fatigue, dyspnea, cognitive dysfunction) lasting weeks to months after the acute infection (commonly referred to as long COVID).
Prevention
  • Vaccination:
    • Vaccination is the most effective preventive strategy. mRNA vaccines (e.g., Pfizer-BioNTech, Moderna) and viral vector vaccines (e.g., Johnson & Johnson) have shown high efficacy in preventing severe illness, hospitalization, and death.
    • Booster doses are recommended to maintain immunity, particularly against emerging variants.
  • Non-Pharmacologic Measures:
    • Masking, social distancing, and hand hygiene remain key strategies to reduce transmission, especially in high-risk settings.
Key Points
  • COVID-19 is caused by SARS-CoV-2, with transmission primarily via respiratory droplets and aerosols. The virus uses the ACE2 receptor for cell entry, leading to multisystem involvement.
  • Symptoms range from mild (fever, cough, anosmia) to severe (dyspnea, pneumonia, ARDS), with complications such as thromboembolism, cardiovascular issues, and multi-organ failure.
  • Diagnosis is confirmed with RT-PCR testing, and imaging may show ground-glass opacities in severe cases.
  • Management includes supportive care for mild cases, with antivirals and monoclonal antibodies used in early disease for high-risk patients. Severe cases may require hospitalization, corticosteroids, antivirals, and immunomodulators.
  • Prevention focuses on vaccination, which remains the most effective tool to prevent severe disease and death.

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