Shock - Pathology
With Diagrams and Explanations (Ref:
Robbins Pathologic Basis of Disease)
Definition of Shock
• Shock is a state of circulatory failure that
results in inadequate cellular oxygen
utilization.
• It leads to tissue hypoxia and cellular
dysfunction.
• Causes include severe hemorrhage, infections,
trauma, or myocardial infarction.
Classification of Shock
• 1. Hypovolemic Shock - due to blood/plasma
loss.
• 2. Cardiogenic Shock - due to pump failure
(e.g., MI).
• 3. Distributive Shock - includes:
• a. Septic Shock
• b. Anaphylactic Shock
• c. Neurogenic Shock
• 4. Obstructive Shock - e.g., pulmonary
Pathophysiology of Shock
• • Decreased tissue perfusion → Cellular
hypoxia.
• • Shift to anaerobic metabolism → Lactic
acidosis.
• • Cell membrane dysfunction → Cell injury.
• • Inflammatory mediator release →
Worsening shock.
Stages of Shock
• 1. Initial Stage: Hypoperfusion, no clinical
signs.
• 2. Compensated Stage: Activation of SNS,
tachycardia, vasoconstriction.
• 3. Progressive Stage: Worsening
hypoperfusion, acidosis, organ dysfunction.
• 4. Irreversible Stage: Severe hypoxia, multiple
organ failure, death.
Morphological Changes in Shock
• • Lungs: Congestion, alveolar damage.
• • Kidneys: Acute tubular necrosis.
• • Heart: Focal necrosis.
• • Liver: Centrilobular necrosis.
• • Brain: Ischemic injury.
Septic Shock - Key Features
• • Common cause of death in ICU patients.
• • Due to systemic infection → Inflammatory
response → Vasodilation.
• • Widespread endothelial activation → DIC
and multiorgan dysfunction.
• • Key mediators: TNF-α, IL-1, IL-6, Nitric oxide.

Pathology_of_Shock_PPT.pptx____hafizur rah

  • 1.
    Shock - Pathology WithDiagrams and Explanations (Ref: Robbins Pathologic Basis of Disease)
  • 2.
    Definition of Shock •Shock is a state of circulatory failure that results in inadequate cellular oxygen utilization. • It leads to tissue hypoxia and cellular dysfunction. • Causes include severe hemorrhage, infections, trauma, or myocardial infarction.
  • 3.
    Classification of Shock •1. Hypovolemic Shock - due to blood/plasma loss. • 2. Cardiogenic Shock - due to pump failure (e.g., MI). • 3. Distributive Shock - includes: • a. Septic Shock • b. Anaphylactic Shock • c. Neurogenic Shock • 4. Obstructive Shock - e.g., pulmonary
  • 4.
    Pathophysiology of Shock •• Decreased tissue perfusion → Cellular hypoxia. • • Shift to anaerobic metabolism → Lactic acidosis. • • Cell membrane dysfunction → Cell injury. • • Inflammatory mediator release → Worsening shock.
  • 5.
    Stages of Shock •1. Initial Stage: Hypoperfusion, no clinical signs. • 2. Compensated Stage: Activation of SNS, tachycardia, vasoconstriction. • 3. Progressive Stage: Worsening hypoperfusion, acidosis, organ dysfunction. • 4. Irreversible Stage: Severe hypoxia, multiple organ failure, death.
  • 6.
    Morphological Changes inShock • • Lungs: Congestion, alveolar damage. • • Kidneys: Acute tubular necrosis. • • Heart: Focal necrosis. • • Liver: Centrilobular necrosis. • • Brain: Ischemic injury.
  • 7.
    Septic Shock -Key Features • • Common cause of death in ICU patients. • • Due to systemic infection → Inflammatory response → Vasodilation. • • Widespread endothelial activation → DIC and multiorgan dysfunction. • • Key mediators: TNF-α, IL-1, IL-6, Nitric oxide.