Inflammation Flashcards

1
Q

What are the body’s defence mechanisms

A
  1. Skin & Mucous membranes - prevent entry of harmful substances (via blink reflex/eyelashes/tears/enzymes/skin etc.)
  2. Inflammation - rapid, non-specific response
  3. Immunity - slow, specific response
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2
Q

Signs of Inflammation

A
  1. Redness (rubor) - caused by vasodilation
  2. Swelling (tumor) - via increased vascular permeability
  3. Heat (calor) - vasodilation
  4. Pain (dolor) - nerve endings = compressed or sensitised by swelling/chemicals
  5. Loss of function - due to tissue damage/pain/swelling
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3
Q

Purpose of inflammation

A
  1. Destroy/ dilute/ isolate injurous agent and damaged tissue
  2. Prevents minor infection from becoming major
  3. Prepares the tissue for repair process.
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4
Q

Causes of Inflammation

A
  1. Injury/Trauma - physical/thermal/chemical etc.
  2. Infection - virus/bacteria/fungi etc.
  3. Infarction - lack of o2
  4. Immune reactions - allergies/ protein insensitivity/ auto-immune responses
  5. Nutrient deprivation
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5
Q

Vascular Response of Inflammation

A
  1. Transient Vasoconstriction- automatic short term narrowing of the blood vessels - contains pathogen/foreign material
  2. Prolonged Vasodilation - allows more cells to arrive and fight infection & dilutes pathogen (causes rubor and calor)
  3. Increased Vascular Permeability - increased blood pressure in area pushes capillary cell wall open
  4. Crenallation - bradykinin causes endothelial retraction so gaps in capillary cell wall get larger.
  5. Plasma Leakage - leave capillary via bigger gaps (tumor)
  6. Haemoconcentration - blood is thicker due to loss of proteins causing stasis - slowing of blood flow.
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6
Q

Cellular Response in Inflammation

A
  1. leukocytes emigrate to area (neutrophils 1st then monocytes).
    - Margination - move to outside of blood flow (caused by chemical attraction and + charge of damaged tissue)
    - Rolling - more resistance on edge - move slower
    - Adhesion - stick to edge
    - Pavementing - Flatten out
    - Chemotaxis - endothelial gaps get larger
    - Pseudopod - projection pushes through gap
    - Amoeboid action - “wriggles” through
    - Emigration via diapedesis - “Cell Walking” leaves blood vessel
    - Chemotaxis - releases chemicals that attract other leukocytes.
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7
Q

4 stages of inflammation

A
  1. Vascular response
  2. Cellular response
  3. Phagocytosis - monocytes become macrophages after diapedesis; engulf pathogens/foreign material/ damaged material
  4. Lymphatic drainage - lymph vessels open + drain excessive fluid/products of inflammation/remaining antigens (presented to immune cells - may trigger immune respomnse)
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8
Q

Acute vs Chronic inflammation

A

ACUTE

  • rapid onset and deterioration
  • usually known cause
  • resolves
  • mainly involves neutrophils and monocytes
  • full function is restored

CHRONIC

  • Slow onset and deterioration
  • Doesn’t resolve
  • Macrophages and fibroblasts
  • Scar tissue formation - function is reduced
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9
Q

Blood tests for acute inflammation

A
  1. White Blood Cell count - increased
  2. Erythrocyte sedimentation rate - increased fibrinogen levels - faster RBC clumping
  3. C-reactive protein levels - increased but may settle down in chronic cases.
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10
Q

Treatments for Inflammation

A
  1. Aspirin - reduces lipids released by damaged tissue
  2. NSAIDs - “ “
  3. Corticosteroids - Interrupt inflammatory process by stopping chemotaxis and phagocytosis
  4. Immunosuppressants - stops out of proportion white blood cell activity (non-specific so can leave vulnerable to other pathogens)
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