Inflammation

Question 1

Why is inflammation important?

Answer 1

• Cell injury initiates body’s response. It’s part of healing process
• Purpose: Remover of injurious agent, remove debris, initiate healing process, anti-inflammatory process, restoration of structure and function
• Vascular and cellular responses (overlapping responses)

Question 2

Acute Inflammation

Answer 2

Sudden and short duration stress

Vascular alterations

Cellular changes

Chemical mediators do inflammation

Leukocyte accumulations

Phagocytosis

Question 3

Vascular Changes

Answer 3

• Goal is to increase fluids, proteins and bloods cells
• Initial Vasoconstriction (Comes first!): Due to nerve reflex
  
  • Ex: Pain nerve endings, release some substance such as serotonin causes constriction
• Main Characteristics
  
  • Vasodilation
  • Increases capillary permeability facilitates movements of leukocytes and plasma proteins
  • Low viscosity due to increased RBCs
  • Clotting in interstitial fluids
• • We use ice to try to cause vasoconstriction because we don’t want to have too many things come to swell

Question 4

Exudate

Answer 4

• Fluid with high protein, cellular debris, high specific gravity
• Types of Exudates
  
  • Hemorrhagic
    
    • Refer patient before treatment
  • Serosanguineous
    
    • Refer patient before treatment
  • Serous
    
    • Can treat patient
    • Thin, clear yellow or straw colored
  • Purulent
    
    • Refer patient before treatment
  • Catarrhal
    
    • Can continue treatment
    • Thin clear mucus

Question 5

Transdute

Answer 5

• fluid with low proteins, no or little cells, low specific gravity
• No endothelial gap, due to pressure

Question 6

Effusion

Answer 6

(mix of exudate and transdate) - Fluid escapes into the anatomical spaces

Ex: Arthritis, Joint spaces

Question 7

Inflammation/Cardinal Signs

Answer 7

• Redness
• Heat
• Edema
• Pain
• Loss of Function
• Pus Formation

Question 8

Lymphatics

Answer 8

• Helps regulate circulatory system
• Initial
  
  • Go through endothelium (thin), anchoring filaments pull and open more to allow fluid in to go to vascular system

Question 9

Initial lymphatic drug inflammation

Answer 9

• Compress lymphatic system through movement
• Need to have exercise for proper lymphatics
  
  • Ex: Patient doesn’t want to get up and exercise
    
    • Explain moving can help reduce swelling

Question 10

Lymphangitis

Answer 10

• Inflammation of lymphatics
• See lymph node enlargement
• Do I need to refer or can I treat?
  
  • Refer if doc doesn’t know

Question 11

Chemical mediators of inflammation

Answer 11

Pathogen and dead cell → Activate mediators of cell death → Cell derived and plasma derived mediators

Cell derived: Mast cells (histamine), Platelets (serotonin)

Question 12

Platelets and Activating Factors

Answer 12

• Activated Platelet and PAF - secretion (Serotonin and Histamine)
• Leukocytes adhesion, margination, and chemotaxis
• Platelet aggregation
• Vasoconstriction, Vasodilation and Bronchoconstriction

Question 13

Serotonin

Answer 13

Causes Vasoconstriction

Platelets store

Question 14

Histamine

Answer 14

• Increases endothelial constriction
• Relaxes mooth muscles of blood vessels
  
  • Both endothelial cell contraction and smooth muscle cell relaxation in blood vessels causes vasodilation
• Cause bronchoconstriction in bronchi and GI and uterus
• Occurs quickly but short lived (inactivated in 30 minutes)

Question 15

Leukocyte Accumulations - Leukocyte adhesion, margination and chemotaxis

Answer 15

• RBC leaves through vascular into endothelial cell, travels through cell to get through to pathogen source
• Margination: attach to endothelial cell, leak through cell.
• Diapedesis: Leukocytes oozes through endothelial openings to interstitial space
• Chemotaxis: Go to pathogen site
• Attack pathogens in two ways
  
  • Release Lactoferrin (bind with iron, reduce iron availability to pathogens)
  • Direct cryptopathic effect by releasing Defensin

Question 16

Leukocyte Accumulations

Answer 16

• Leukocytes lifespan is 24 hours
• Sometimes neutrophil prolonged response response
• First to get there
• After 24 hours: Increase Machrophages to clean up cellular debris including leukocytes
• Leukocytes – remove pathogens and release growth factors for healing

Question 17

Arachidonics Acid Derivatives

Answer 17

• Arachadonic Acids
  
  • Cyclooxygenase
    
    • Prostaglandins
      
      • Can do vasoconstriction or vasodilation
  • Lipoxygenase pathways
    
    • Leukotrienes

Question 18

Selective COX inhibition (Prostoglandins)

Answer 18

• COX1
  
  • Normal constituent of cells
  • Synthesize to protect cell and their function
• COX2
  
  • Injury of infection
  • Fever
  • Produces PGs that can cause pain, inflammation and fever
    
    • Ex: RA

Question 19

Giving NSAIDS to stop COX2

Answer 19

• Carticosteroids stop Arachidonic Acid from being made
• Effect the enzymes so it won’t be produced
• Too much NSAIDS
  
  • Leads to other issues
    
    • Try different medications
    • Ex: Celecoxib (Non traditional NSAID)
      
      • Only effects COX2 inflammation
        
        • NSAID
    • Aspirin
      
      • Traditional
      • Effects both pathways

Question 20

What happens with COX2?

Answer 20

• Can increase risk for cardiovascular condition
• Normal
  
  • COX 1 PGS = Platelets and Vasoconstriction
  • COX 2 PGs = Vasodialation
• Problem with COX-2 Selective drugs: Increase VC, platelet activity
  
  • Evidence of heart attack or stroke
  • Increase clumping of platelets

Question 21

Leukotrienes

Answer 21

Like histamine

Increases smooth muscle contraction - Bronchoconstriction

Question 22

Cytokines

Answer 22

Promote inflammation, help with inflammation

Question 23

ILF

Answer 23

• In brain (fever)
• Help body fight of pathogens through inflammation
• Too much inflammation leads to shock
• In Liver (C-Reactive Proteins)
• In circulation (Increased neutrophils, decreased lymphocytes)

Question 24

Phagocytosis of bacteria

Answer 24

• Attaches, hugs and consumes bacteria
  
  • Macrophage
• Enzymes inside kills bacteria

Question 25

Plasma Proteins (proteases) Systems

Answer 25

Cell injury or toxin → Activate plasma protein systems Systems * Blood coagulation and fibrinolytic system * Kinin System * Complement System

Question 26

Blood Coagulation

Answer 26

1. Platelet 1. Place clot 2. Enzyme thrombin 3. Fibrinogen 4. Fibrin 1. Traps, exudate microbes

Question 27

Firbinolytic

Answer 27

1. Tissues 1. Tissues plasminogen activator 2. Plasminogen 3. Enzyme plasmin 4. Splits fibrin 5. Fibrin degradation 6. Chemotaxis for leukocytes, increase vascular permeability

Question 28

Kinin System

Answer 28

* Activated by Hageman Factor (Clotting Factor 7) * Activates Factor 7 * Bradykinin creates Vasodilation * Brady means slow * Assists in inflammatory response

Question 29

Complement Systems

Answer 29

* Activated in microorganism and anitgen-antibody complex * Combine cause inflammation * Plasma protein fragments * Membrane attack complex * Splits into two complexes * **C3a, C5a** * **Take WBCs to come and see cell; need to do something** * **Work with Mast Cells** * **Let Leukocytes come and go to do there job -\> enhance inflammation** * C5b to C9 * Kill pathogen * Opens cell to allow for Na and water to go into cell * Opsonization C1 to C3b * (coating of microbes for phagocytosis – Macrophages) **Tagging!**