Diabetes and COVID Flashcards
Why are poor outcomes of COVID-19 associated with diabetes?
Compromised immune responses and Chronic inflammation of multiple organ systems
What is the mortality rate for COVID-19 associated with diabetes?
Without health conditions: about 1% -> 10x more than influenza
With diabetes: 7.3%
What are the risk factors for COVID-19?
-Age
-Male gender
-pre-existing health conditions like heart disease and diabetes
What are risk factors that increase the severity of COVID-19?
-Age
-Male gender
-health conditions like heart disease and diabetes
-obesity
-hypertension
Why is Diabetes such a risk factor?
CYCLE
-Chronic inflammation and weak immune response make patients prone to COVID-19 infection + poor outcome
-> COVID worsens diabetes by increasing insulin resistance and decreasing insulin production
How does diabetes interfere with immune responses?
-Hyperglycemia inhibits chemotaxis, adhesion, and diapedesis of neutrophils -> they can’t get from blood vessels to the site of infection
-hyperglycemia also inhibits phagocytosis, degranulation, NET formation (traps)
What causes diseases in multiple organs associated with diabetes?
Systemic and tissue inflammation
CVD = cardiovascular disease
DKD = diabetic kidney disease
DR = diabetic retinopathy
NASH = nonalcoholic steatohepatitis
Obesity can also increase inflammation
What is the cut-off BMI for obesity?
Obesity when above 35
What are the consequences of loss of glycemic control, indicated to be caused by COVID-19?
-Insulin resistance
-Impaired insulin secretion
Where are ACE-2 receptors found (target of COVID-19)
in endothelial cells of blood vessels of multiple organs -> heart, kidney, brain, lungs
What is the risk of COVID-19 binding to ACE-2 receptors?
Immune response -> Cytokine storm and coagulation in
the lung: ARDS (Acute respiratory distress syndrome)
heart: myocardial infarct (MI)
brain: stroke
pancreas
What are consequences of COVID-19 binding to ACE-2 receptors regarding to the Renin-Angiotensin system?
Angiotensinogen (from liver) cleaved by Renin (from the kidney) to form Angiotensin I -> ACE-1 converts it to Angiotensin II -> ACE-2 converts Angiotensin II to Angiotensin 1-7 preventing negative outcomes
COVID-19 block ACE-2, causing an excess of Angiotensin II and less of Angiotensin 1-7
too much Angiotensin II causes: vasoconstrictor, inflammation, fibrosis, lung damage, edema
How does Angiotensin 1-7 prevent negative outcomes of high levels of Angiotensin II?
Angiotensin 1-7 activates Mas:
Vasodilation, vasoprotection, lung damage, and edema inhibition