It displays Covid pathophysiology, diagnosis, symptoms and treatment.

1. Infections and Infestation
Study of Coronavirus (SARS CoV 2)
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Pathogenesis, Pathology & Lab
Findings of COVID 19
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MBBS 2nd Year – Pathology Group
Discussion

2. Overview of Coronaviruses
• Coronaviruses: Enveloped, positive sense
‑
single stranded RNA viruses.
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• Genome: ~30 kb, largest among RNA viruses.
• Four genera: Alpha, Beta (pathogenic to
humans), Gamma, Delta.
• Human infections range from common cold to
severe diseases like SARS, MERS, and
COVID 19.
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3. SARS CoV 2 Structure (Detailed)
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• Spike (S) protein: Mediates attachment and
fusion; primary virulence determinant.
• Receptor-binding domain (RBD) binds ACE2
receptors.
• Membrane (M) and Envelope (E) proteins:
Essential for viral assembly.
• Nucleocapsid (N) protein: Binds RNA genome;
important for replication.
• Lipid envelope: Sensitive to disinfectants.

4. Virus Replication Cycle
• 1. Attachment: S protein binds ACE2 receptor.
• 2. Endocytosis or membrane fusion.
• 3. Release of viral RNA into cytoplasm.
• 4. Translation of ORF1a/1ab → polyproteins →
cleaved into NSPs.
• 5. Formation of replication–transcription
complex (RTC).
• 6. Genome replication and subgenomic mRNA

5. Transmission & Risk Factors
• Highly contagious through droplets, aerosols,
and fomites.
• Super spreader events major driver.
‑
• Risk factors: Age > 60, diabetes, hypertension,
cardiovascular disease, obesity,
immunosuppression.
• Pregnancy and chronic lung diseases increase
severity.

6. Pathogenesis – Early Phase
• Virus enters via respiratory mucosa.
• Infects type II pneumocytes and upper airway
epithelial cells.
• ACE2 down regulation → loss of protective
‑
signaling.
• Local inflammation with neutrophils and
macrophages recruitment.
• Direct cytopathic effect causes epithelial cell
death.

7. Pathogenesis – Immune
Dysregulation
• Hyperinflammatory response (“cytokine
storm”).
• ↑ IL 6, IL 1β, TNF α, interferons.
‑ ‑ ‑
• Widespread endothelial activation → capillary
leak.
• Systemic inflammatory response contributes
to ARDS and multi organ failure.
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8. Pathogenesis – Coagulopathy
• SARS CoV 2 induces endothelial injury →
‑ ‑
activation of coagulation pathways.
• Microvascular thrombosis and DIC like picture.
‑
• Elevated D dimer and fibrin degradation
‑
products.
• Pulmonary embolism and stroke observed in
severe cases.

9. Gross Pathology of Lungs
• Heavy, congested, edematous lungs.
• Patchy to diffuse consolidation.
• Hemorrhagic areas in severe cases.
• Evidence of microthrombi.

10. Microscopic Pathology of Lungs
• Diffuse alveolar damage (exudative phase):
• • Hyaline membrane formation.
• • Interstitial and intra alveolar edema.
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• • Type II pneumocyte hyperplasia.
• Later proliferative/organizing phase:
• • Fibroblast proliferation.
• • Interstitial fibrosis.
• • Vascular microthrombi.

11. Other Organ Pathology
• Heart: Myocarditis, microvascular injury.
• Kidneys: Acute tubular necrosis,
microthrombi.
• Liver: Mild hepatitis, cholestasis.
• Brain: Hypoxic injury, microhemorrhages.
• Blood vessels: Endotheliitis and thrombosis.

12. Clinical Features – Expanded
• Asymptomatic to critical illness.
• Common: Fever, dry cough, sore throat,
myalgia, anosmia.
• Moderate: Pneumonia without severe
hypoxia.
• Severe: Respiratory failure, ARDS, shock,
multi organ dysfunction.
‑
• Long COVID: Persistent fatigue, dyspnea,
cognitive dysfunction.

13. Laboratory Findings – Hematologic
• Lymphopenia: hallmark finding.
• Neutrophilia in severe disease.
• Thrombocytopenia in some cases.
• Elevated NLR (Neutrophil Lymphocyte Ratio)
‑
correlates with severity.

14. Laboratory Findings –
Inflammatory Markers
• CRP: Markedly elevated.
• Ferritin: Hyperferritinemia indicates cytokine
storm.
• IL 6: Elevated in severe cases.
‑
• Procalcitonin: Normal initially; elevated
suggests bacterial co infection.
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15. Laboratory Findings – Coagulation
& Biochemistry
• D dimer: Elevated; predicts thrombotic risk.
‑
• Fibrinogen: Elevated early, decreased in late
DIC.
• LFTs: Mild elevation of AST/ALT.
• Renal markers: Increased urea/creatinine in
severe disease.

16. Diagnostic Modalities
• RT PCR: Gold standard.
‑
• Detects viral RNA from nasopharyngeal swabs.
• Antigen tests: Quick but less sensitive.
• Antibody tests: Useful for surveillance.
• Imaging: HRCT shows ground glass opacities,
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crazy paving pattern.
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17. HRCT Findings
• Bilateral, peripheral ground glass opacities.
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• Consolidation in later stages.
• Interlobular septal thickening.
• Vascular enlargement in affected areas.
• Associated with severity staging.

18. Summary & Key Points
• SARS CoV 2 causes a multi system disease
‑ ‑ ‑
driven by inflammation and endothelial injury.
• Pathology dominated by diffuse alveolar
damage and microthrombosis.
• Laboratory markers help assess severity and
prognosis.
• Understanding detailed mechanisms essential
for diagnosis and management.