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CLS > Body Response to Inflammation > Flashcards

Body Response to Inflammation Flashcards

1
Q

Function of Acute Inflammatory Response

A

AIR = Most common response of body tissues to nearby damage - Destroy or neutralise damaging agent - Liquefy and remove dead tissue - Prepare damaged area for healing

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2
Q

Situations causing AIR

A
  • Microorganisms - Physical trauma - Ischaemic Necrosis - Radiation damage - Chemical damage
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3
Q

Main steps in AIR

A

Production of AI Exudate:

  1. Vessels dilate due to substances released from damaged tissue e.g. histamine; loss of axial flow pattern
  2. Endothelial cells swell and retracts, vessels leak; increases permeability; allows water, salts, protein(fibrinogen and Ig) to leak into damaged area; tissue becomes oedamatous
  3. Neutrophils marginate and emigrate; Stick to endothelial cells, marginatino. Emigrate through capillary to area of damage
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4
Q

Mediators of AIR

A

Chemokines

Cytokines

Eicosanoids

Adhesion molecules (selectins, integrins)

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5
Q

Composition of AIE

A

Fluid of blood serum

Fibrinogen

Neutrophils

Macrophages(in chronic inflammtion)

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6
Q

Types of AIE

A

Serous:

Fluid rich, Cell poor

e.g. congestive cardiac failure

Purulent

High concentration of leukocytes

e.g. meningitis

Fibrinous

Fibrin cross-links

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7
Q

Specific role of fluid in AIE

A

Dilutes toxins

Carries substances preformed in blood

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8
Q

Function of Neutrophils in AIE

A

Actively phagocytotic of

living tissue; bacteria

necrotic debris; breaks down damaged tissue

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9
Q

Clinical effects/symptoms of AIR

A

Calor = heat

Dolor = pain

Rubor = redness

Tumor = swelling

Malaise, fever, Pain, tachycardia

incr neutrophil count, acute phase proteins and ESR

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10
Q

Possible outcomes of acute inflammation

A
  1. Resolution
  2. Abscess formation
  3. Organisation and repair
  4. Chronic inflammation
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11
Q

Resolution of acute inflammation

A

AIE eliminates damaging agents completely

Macrophages remove dead cells and exudate

Local cells re-grow; function returns to normal

e.g. Pneumonia

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12
Q

Abcsess formation as result of Acute inflammation

A

= A large accumulation of liquid purulent in an area where tissue damage has led to extensive necrosis

Becomes walled off in attempt to limit spread

Especially caused by bacteria

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13
Q

Healing by repair in response to Acute inflammation

A
  1. Tackling debris by macrophages, area becomes semi liquid.

vascular: Capillaries grow into area

fibrovascular: Fibroblasts lay down collagen fibres but also capillaries

collagenous: Reduced vascularity. large amount of collagen fibre

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14
Q

Definition of chronic inflammation

A

Inflammation that may have rapid or slow onset, but characterised primarily by its persistence and lack of clear resolution; occurs when the tissues are unable to overcome the injuring agent

Damaging stimulus cant be removed

Or Complete healing cant occur

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15
Q

Pathological features of chronical inflammation

A
  • Continued inflammation
  • Damage occuring together with organisatino and repair
  • Macrophage is main effector cell
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16
Q

Role of macrophages in chronic inflammation

A

Activated by interferon-y

- Phagocytotic role

- Secretory role:

proteases

hydrolases

Growth factors -> healing response

Inflammatory mediators->immune response

IL-1, TNFa

17
Q

3 outcomes of chronic inflammation

A
  1. Improvement
    • Stimulus removed or neutralised
    • Healing gains upper hand, scarring completes e.g. peptic ulcer
  2. Stalemate
    • Continuing damage and reapir
    • Cant complete scarring
  3. Worsening
    • Stimulus increases or impaired healing
    • Damage too extensive for repair
18
Q

Definition granulomatous inflammation

A

Form of inflammation where neutrophils are ineffective so macrophages are involved early on

If organism low pathogenicity, or resistant to neutrophils = type IV

Granuloma = fusion of macrophages

Interaction with T cells

19
Q

Main stages of wound healing

A

Inflammatory: 2-5 days

Haemostasis, inflammation

Proliferation: 3d-3weeks

Granulation tissue bridges defect, contraction, epithelialisation

Remodelling: 3w-2y

New collagen->incre tensile strenght

20
Q

Healing by primary intention

A
  • clean incision
  • edges cloesely apposed
  • minimal exudate
  • no wound infection

Results in granulation itssue, matures to clean collagenous scar

21
Q

Healing by second intention

A
  • Extensive damage/tissue destruction
  • Wound edges cant be approximated
  • +/-infection

Result

  • Greater amount of necrotic debris
  • Greater amount of tissue remodelling
    • Larger area of necrosis, worse scars
22
Q

Disadvantages of AIE

A

AIE can have secondary effects

  • e.g. meningitis, increased intracranial pressure
  • Pericarditis
  • Pleurisy, fibrous AIE in lungs, rubbing
  • Peritionitis etc
23
Q

Factors leading to inadequate healing

A

ISchaemia

Continuing infection

Diabetes

Denervation

Steroid therapy

24
Q

Repair process in brain

A

Cant make collagen, instead:

Macrophages cause liquefication, phagocytose debris and tissue dies

Astrocytes proliferate and lay down glial fibres, wall off area, limit damage

25
Q

Repair in bone

A

Collagen itself not strong enough, needs to lay down new bone

  1. Defect filled with haematoma
  2. Phagocytosis of debris; haematoma undergoes organisation; defect filled with granulation tissue, first vascular, then fibrovascular; osteoprogenitor cells develop
  3. Become osteoblasts and synthesise osteoid collagen; calcifies to woven bone
  4. Woven bone links up with old bone
  5. Remodelling continues
26
Q
A

CLS (20 decks)

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