COVID-19 and Elderly

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Salient Points

In this Indian Journal of Geriatric Care, it lists out the following:

  • Various etiology,
  • Pathophysiology of COVID-19 as well as the,
  • Pathogenesis of disease.

Clinical features and the evaluation of COVID-19 patients, treatment protocols and prevention have also been discussed.

COVID-19 in the elderly with comorbidities such as:

  • Diabetes
  • Hypertension
  • Sleep problems
  • COPD
  • Asthma

The journal also discusses prospective vaccinations, Japan, United Kingdom, Nepal as well as Wuhan’s experience in dealing with the pandemic,

Detailed Summary

Etiology

  • Coronavirus belongs to a large family of enveloped ssRNA viruses.
  • They are divided into 4 genera: alpha, beta, delta, gamma.
  • Alpha and Beta genera are known to infect humans.
  • Incubation period – 1 – 14 days (around 5 days)
  • R/F – CFR highest in those with multiple comorbidities, travel history to the countries with corona epidemic, close contact with a suspect case and those with low immunity.
  • Host Factors – Age above 70 years with median age of 51 years old, 51% affected individuals are male.
  • Mode of transmission – Droplets, aerosols, fomites.
  • Environmental Factors – Winters and temperature of more than 27C would disrupt the structure of the virus.

Pathophysiology

  • COVID-19 infection is capable of producing an excessive immune reaction in the host.
  • The reaction is known as Cytokine Storm – causes extensive tissue damage, mediated by IL-6.
  • IL-6 is produced by activated leukocytes and acts on a large number of cells and tissues.
  • It promotes the differentiation of B cells, promotes growth of some cells and inhibits the growth of others. It also stimulates the production of Acute Phase Proteins.
  • IL-6 is associated with an Acute Systemic Inflammatory Syndrome – fever + MOD
  • Structural analysis suggests that the virus binds to ACE-2 Receptors in humans, suggesting a similar pathogenesis to SARS.
  • Evidence also points to the virus attacking alveoli in the lungs to cause fluid build up and collapse of sections of the lungs.
  • The virus also appears to reduce the O2 carrying capacity of RBCs, hence patients with CVS disease and DM have a higher risk of complications.

Pathogenesis

  • Infection begins when the viral spike glycoprotein attaches to its complementary host cell receptor.
  • After attachment, a protease of the host cell cleaves and activates the receptor attached spike protein.
  • Activation allows the virus to enter the host cell by endocytosis or by direct fusion of the viral envelope with the host membrane.
  • The virus requires an ACE2 receptor to enter the cells.
  • On entry, the virus particle is uncoated and its genome enters the cell cytoplasm.
  • The viral RNA genome attaches to the host cell’s ribosome for translation.
  • The host ribosome translates the initial overlapping open reading frame of the viral genome which forms a long polyprotein.
  • The polyprotein has its own proteases which cleave the polyprotein into multiple non structural proteins.
  • A number of NSP like RNA dep RNA polymerase and Exoribonuclease lead to replication and transcription of RNA. RNA translation occurs inside the ER and progeny viruses are released from the host cell by exocytosis through secretory vesicles.

Clinical Features

  • R/F – Older patients with DM, Chronic Lung Disease, CVS disease and compromised immune systems.
  • Clinical features
  1. Fever
  2. Small frequent bouts of cough
  3. Breathlessness
  4. Pressure in the chest
  5. Fatigue
  6. Sore throat
  7. Diarrhoea
  8. Laryngitis
  9. Loss of Smell and Taste
  10. Cervical Lymphadenopathy

Clinical Syndromes associated with COVID-19

  1. Mild illness
  2. Pneumonia
  3. Severe Pneumonia
  4. ARDS
  5. Sepsis
  6. Septic Shock

Clinical Classification

  1. Mild disease – Uncomplicated respiratory symptoms
  2. Severe disease – Dyspnea, >50% lung involvement on imagine (within 24 or 48hrs)
  3. Critical disease – Respiratory failure, shock, MOD

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