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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Why is inflammation important?

A
  • 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)
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2
Q

Acute Inflammation

A

Sudden and short duration stress

Vascular alterations

Cellular changes

Chemical mediators do inflammation

Leukocyte accumulations

Phagocytosis

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3
Q

Vascular Changes

A
  • 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
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4
Q

Exudate

A
  • 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
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5
Q

Transdute

A
  • fluid with low proteins, no or little cells, low specific gravity
  • No endothelial gap, due to pressure
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6
Q

Effusion

A

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

Ex: Arthritis, Joint spaces

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7
Q

Inflammation/Cardinal Signs

A
  • Redness
  • Heat
  • Edema
  • Pain
  • Loss of Function
  • Pus Formation
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8
Q

Lymphatics

A
  • Helps regulate circulatory system
  • Initial
    • Go through endothelium (thin), anchoring filaments pull and open more to allow fluid in to go to vascular system
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9
Q

Initial lymphatic drug inflammation

A
  • 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
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10
Q

Lymphangitis

A
  • Inflammation of lymphatics
  • See lymph node enlargement
  • Do I need to refer or can I treat?
    • Refer if doc doesn’t know
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11
Q

Chemical mediators of inflammation

A

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

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

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12
Q

Platelets and Activating Factors

A
  • Activated Platelet and PAF - secretion (Serotonin and Histamine)
  • Leukocytes adhesion, margination, and chemotaxis
  • Platelet aggregation
  • Vasoconstriction, Vasodilation and Bronchoconstriction
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13
Q

Serotonin

A

Causes Vasoconstriction

Platelets store

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14
Q

Histamine

A
  • 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)
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15
Q

Leukocyte Accumulations - Leukocyte adhesion, margination and chemotaxis

A
  • 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
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16
Q

Leukocyte Accumulations

A
  • 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
17
Q

Arachidonics Acid Derivatives

A
  • Arachadonic Acids
    • Cyclooxygenase
      • Prostaglandins
        • Can do vasoconstriction or vasodilation
    • Lipoxygenase pathways
      • Leukotrienes
18
Q

Selective COX inhibition (Prostoglandins)

A
  • 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
19
Q

Giving NSAIDS to stop COX2

A
  • 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
20
Q

What happens with COX2?

A
  • 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
21
Q

Leukotrienes

A

Like histamine

Increases smooth muscle contraction - Bronchoconstriction

22
Q

Cytokines

A

Promote inflammation, help with inflammation

23
Q

ILF

A
  • 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)
24
Q

Phagocytosis of bacteria

A
  • Attaches, hugs and consumes bacteria
    • Macrophage
  • Enzymes inside kills bacteria
25
Q

Plasma Proteins (proteases) Systems

A

Cell injury or toxin → Activate plasma protein systems

Systems

  • Blood coagulation and fibrinolytic system
  • Kinin System
  • Complement System
26
Q

Blood Coagulation

A
  1. Platelet
    1. Place clot
  2. Enzyme thrombin
  3. Fibrinogen
  4. Fibrin
    1. Traps, exudate microbes
27
Q

Firbinolytic

A
  1. Tissues
    1. Tissues plasminogen activator
  2. Plasminogen
  3. Enzyme plasmin
  4. Splits fibrin
  5. Fibrin degradation
  6. Chemotaxis for leukocytes, increase vascular permeability
28
Q

Kinin System

A
  • Activated by Hageman Factor (Clotting Factor 7)
    • Activates Factor 7
    • Bradykinin creates Vasodilation
    • Brady means slow
    • Assists in inflammatory response
29
Q

Complement Systems

A
  • 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!

Pathology (7 decks)

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