COVID-19 (Corona Virus Disease 2019): Pathophysiology and Clinical Findings
Authors: Ryan Brenneis, Yan Yu* Reviewers: Ciara Hanly, Yonglin Mai (􏰄􏰁􏰃)*, Stephen Vaughan* * MD at time of publication
-Respiratory failure -Septic shock -Multiple organ dysfunction
Critical
Respiratory droplet production (cough, sneeze, talking, breathing) by human host or animal vector infected with SARS-CoV-2
Note: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the name of the betacoronavirus (a positive sense, single stranded RNA virus). COVID-19 is the name of the disease caused by this virus.
rate, ↓ oxygen saturation -Bilateral interstitial infiltrates on Chest X-ray, progressively worsening
Small droplets (<5μm in diameter) are aerosolized and become airborne Inhalation of aerosolized particles that are suspended in air Patient exposed to the virus (SARS-CoV-2) Droplet contacts the mucus membranes (eyes, nose, mouth) of recipient Live viral particles can adhere to inanimate objects called fomites (e.g. doorknobs) Symptoms are on a continuum -Worsening dyspnea: ↑ respiratory -Fever -Cough -Myalgia, fatigue -Nausea/vomiting -Diarrhea -Loss of taste/smell Recipient touching infected fomite subsequently touches any of their mucus membranes Mild Moderate Severe Virus spreads in the body via 1) mucus membrane spread to surrounding cells and 2) entering the blood Virus adheres to angiotensin-converting enzyme 2 (ACE-2) receptor on body cells, mimics ACE-2, & gains access into cell COVID-19 Symptomatic infection with SARS-CoV-2 Viral proliferation in cells of tissues with more ACE-2 receptors: lungs (type II pneumocytes); vasculature (endothelial cells), kidneys (proximal tubular epithelium), heart (myocardium), GI tract (enterocytes) Cell death and ↑ in inflammatory cytokines triggers immune response Neutrophils move to lungs, release reactive oxygen species and cytokines Alveolar/capillary damage Fluid accumulates in interstitium and alveoli ↑ Distance for O2 to diffuse from alveoli to capillaryà ↓ blood O2 saturation Cytokines induce the hypothalamus to release prostaglandins ↑ body temperature set point to fight infection Virus disassembles, releasing viral RNA, which uses host cell’s ribosomes to make new viral proteins like RNA-polymerases Newly made viral RNA-polymerases use cell’s own nucleotides to synthesize new viral RNA Bilateral ground-glass opacities (CT lung) & interstitial infiltrates on Chest X-ray Dyspnea Airway irritation Cough Myocardial cell damage ↑ Troponin ↑ skeletal muscle cell damage Viral RNA & proteins packaged into new viral particles New virus assembled and released from cell, killing the cell and contributing to disease symptoms Average incubation period (time from initial infection to symptom onset) is 4-5 days; can be up to 14 days Heart tries to compensate for Fever Myalgia hypoxemiaà↑ cardiac output Arrhythmogenic and strain on myocardium state Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published March 22, 2020, updated Aug 18, 2021 on www.thecalgaryguide.com