This is just an educational presentation on Introduction to COVID-19. Can be used to get aware about the disease. and ongoing treatment.

1. Dr. Ayshah Hashimi

2. Introduction
• An infectious disease caused by newly discovered corona virus- SARS CoV-2
• It’s a Zoonotic disease that affect the respiratory system
• In severe cases it causes restrictive lung disease
• It started in 2002 as SARS, then after mutation it came back in 2013 as MERS and now it is back in 2019 as
COVID-19
• First case was reported on 31st December, 2019, in Wuhan city of China
• WHO declared COVID-19 as pandemic on 11th March, 2020
Spread
• Droplet infection
• Faeco-oral route

3. Pathogenesis
• SARs CoV-2 enters the lungs and reaches alveoli
• Gains entry in pneumocyte type II cells through ACE-2 receptors with the help of S-spikes and release its
single stranded RNA molecule
• With the help of ribosomes, the viral RNA undergoes translation and forms polyproteins. These polyproteins
are cleaved into various virus particles by proteinases
• In presence of RNA dependant RNA polymerase, the viral RNA undergoes replication and increases its
number
• This is how SARs CoV-2 multiplies and when it leaves it destroys the pneumocyte
• Damaged pneumocyte releases certain chemical mediators that attracts leucocytes
• Neutrophils reaches first and fights the infection by releasing Reactive oxygen species (ROS) and proteases.
• Alveolar macrophages releases cytokines i.e. IL1, IL2 IL6, IL7, TNF-α etc. that causes vasodilatation, ↑ vascular
permeability

4. ↓ SPO2  chemoreceptor stimulate SNS
↓
↑ Heart Rate and ↑ Respiratory rate
(Tachycardia and Tachypnoea )

5. Effect of Cytokine Storm on different system or Systemic Inflammatory Response Syndrome
• Hypothalamus in response to cytokines (IL1, IL6, TNF-α) releases Prostaglandin E2 responsible for Fever
• Due to ↓pO2 peripheral chemoreceptors send stimulus to brain to activate sympathetic nervous system
to ↑ Heart rate (Tachycardia) and ↑ respiratory rate (Tachypnoea) in order to compensate hypoxemia
• Cytokine storm causes vasodilation  ↓ Blood volume  ↓Total Peripheral Resistance  ↓ Blood
Pressure ↓ Perfusion to different organs
• ↓ Perfusion to Kidney causes  ↑BUN & ↑ S. Creatinine
• ↓ Perfusion to Liver causes  ↑AST, ↑ ALT, ↑Bilirubin
↑Acute phase Reactive Proteins (Fibrinogen, IL6, CRP)
• ↓ Perfusion to Heart causes  ↑ Troponin I & T
↑ CK- MB

6. Sign & Symptoms
• Fever (≥100.4)
• Productive Cough
• Shortness of Breath (Dyspnea)
• Symptoms of URTI (Rhinorrhea, Congestion, sore throat)
• Symptoms of GIT (Nausea Vomiting, Diarrhoea)
Differential Diagnosis
• Flu
Nasopharyngeal/ oropharyngeal swab Taken for RT-PCR or NAAT
Vitals
• Blood pressure decreased
• Heart Rate Increased (>100bpm)
• Respiratory rate Increased (>22bpm)
• Fever (>100.4°F)

7. Physical Examination
Auscultate
• Bronchial sounds ratifies consolidation
• Wheezing shows obstruction
• Rhonchi
• Crackles denotes accumulation of fluid
Investigations
Complete Blood Count (CBC)
• Lymphopenia
 Direct lysis of cells by SARs CoV-2 because Lymphocytes has ACE-2 receptors
 Apoptosis of lymphocytes due to cytokine storm
 Cytokine storm causes atrophy of lymphoid organ thus there is decrease lymphocyte turnover
 Lactic acid acidosis that inhibits lymphocyte proliferation

8. • Neutrophilia
• Raised ESR
• CMP (Comprehensive Metabolic Panel) includes BMP and LFT
 LFT- Raised AST, ALT, T. Bilirubin and Acute phase reactive proteins (CRP, IL6, Fibrinogen, Ferritin)
 BMP checks Fluid/electrolyte imbalance and Kidney function
 Raised BUN, S. Creatinine and decreased T. Protein
 Na, K, Ca, Cl, CO2, CHO
• Raised Troponin I/T and CK-MB
• ECG
 Arrythmia
 Prolonged QT interval
 STEMI
 NSTEMI

9. • Raised procalcitonin indicates bacterial infection
• Cytokine storm causes activation of pro-coagulants and inhibits anti-coagulants
• Raised PTT and PT/INR  Increased formation of Clot
• Initially fibrinogen increases and later on decreases
• Increased D-Dimers indicates a patient prone to DIC (Disseminated Intravascular Coagulation)
• Increase level of Lactate Dehydrogenase (LDH) indicates severity of the disease or multiple organ failure
ABG (Arterial Blood Gas)
• Initially respiratory alkalosis
↑ RR  ↓CO2  ↓ Hᶧ  pH ↑
• Then, Respirator acidosis
↑ CO2  ↑ Hᶧ  pH ↓
• Later on metabolic acidosis
↑ CO2  ↑ Hᶧ  pH ↓ + ↓ ↓ HCO3ֿ

10. Radiology
• X- ray opacities visible
• CT- Scan
 Ground glass Opacities
 Crazy paving patterns
 Consolidation with Air Bronchogram

11. Treatment
• IV infusion (RL, NS) given sparingly
• Paracetamol
• Remdesivir (RNA dependant RNA Polymerase inhibitor)
• Chloroquine and hydroxychloroquine (Entry inhibitor or Endocytosis Blocking Agent) promising results
observed in vitro studies but in clinical trials the results were very discouraging also there were serious side
effects (conduction disorder in heart, rash, vomiting headache etc.)
• Ritonavir (protease inhibitor)
• Tocilizumab (Immunosuppressive) recombinant humanized monoclonal antibody against IL6 (Dose 8mg/kg)
Side effects- rhinorrhoea, sore throat, sinus pain, common cold, headache, GI- perforation in long term use
• Corticosteroids (only prescribed to patients with severe ARDS)
• Vaccine

12. Mechanical ventilation in ARDS
• AC Volume method
 ↓ Tidal Volume
 ↑ Respiratory rate
 ↑ PEEP (positive end-expiratory pressure)
• AC Pressure method
• Bilevel ventilation
• Airway pressure release ventilation
• Extracorporeal membrane oxygenation (ECMO)

13. COVID-19 Prevention