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Review
. 2021 Sep:69:102745.
doi: 10.1016/j.amsu.2021.102745. Epub 2021 Aug 23.

Coronavirus disease 2019 (COVID-19): Multisystem review of pathophysiology

Tanveer Mir  1 , Talal Almas  2 , Jasmeet Kaur  3 , Mohammed Faisaluddin  4 , David Song  5 , Waqas Ullah  6 , Sahil Mamtani  7 , Hiba Rauf  8 , Sunita Yadav  9 , Sharaad Latchana  10 , Nara Miriam Michaelson  11 , Michael Connerney  12 , Yasar Sattar  13
Affiliations
Review

Coronavirus disease 2019 (COVID-19): Multisystem review of pathophysiology

Tanveer Mir et al. Ann Med Surg (Lond). 2021 Sep.

Abstract

Coronavirus disease-19 (COVID-19) pandemic is associated with high morbidity and mortality. COVID-19, which is caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS CoV-2), affects multiple organ systems through a myriad of mechanisms. Afflicted patients present with a vast constellation of symptoms, from asymptomatic disease to life-threatening complications. The most common manifestations pertain to mild pulmonary symptoms, which can progress to respiratory distress syndrome and venous thromboembolism. However, in patients with renal failure, life-threatening cardiac abnormalities can ensue. Various mechanisms such as viral entry through Angiotensin receptor (ACE) affecting multiple organs and thus releasing pro-inflammatory markers have been postulated. Nevertheless, the predictors of various presentations in the affected population remain elusive. An ameliorated understanding of the pathology and pathogenesis of the viral infection has led to the development of variable treatment options, with many more that are presently under trial. This review article discusses the pathogenesis of multiple organ involvement secondary to COVID-19 infection in infected patients.

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Conflict of interest statement

None.

Figures

Fig. 1
Fig. 1
Pathogenesis of the procoagulant state secondary to COVID-19.
Fig. 2
Fig. 2
The mechanisms underlying SARS-CoV-2 induced ARDS [1] a hypothetical model of SARCoV-2 virus demonstrating infectious pathways to cell entery, induce inflammation, ARDS and procoagulation state. SARS CoV-2; Severe Acute Respiratory Syndrome Coronavirus-2, IL-6; Interleukin −6, TNFα; Tumor necrosis alpha, IL 1-β; Interleukin 1-beta, ACE II; Angiotensin converting enzyme II, Ang II; Angiotensin II (Created with BioRender.com).
Fig. 3
Fig. 3
Pathogenesis underlying the acute kidney injury (AKI) seen in SARS-CoV-2. SARS CoV-2; Severe Acute Respiratory Syndrome Coronavirus-2, IL-6; Interleukin −6, TNFα; Tumor necrosis alpha, IL 1-β; Interleukin 1-beta, ACE II; Angiotensin converting enzyme II, Ang II; Angiotensin II (Created with BioRender.com).
Fig. 4
Fig. 4
Cardiovascular pathology of COVID-19. SARS CoV-2; Severe Acute Respiratory Syndrome Coronavirus-2STEMI; ST-elevation myocardial Infarction, NSTEMI; Non-ST elevation myocardial infarction (Created with BioRender.com).
Fig. 5
Fig. 5
Pathogenesis of myocarditis in COVID-19 infection.
Fig. 6
Fig. 6
Neurologic involvement in COVID-19.
See this image and copyright information in PMC

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